Namibian Didge Lessons

As a kid growing up in rural Australia I was fascinated by the prehistory of our continent.  The ancient Aboriginal stories and creation myths permeated our Western culture.  The opportunity to play the “didge” came up whenever we discovered a discarded length of PVC tube or Mum’s vacuum cleaner pipe laying around.  For those of you who are not familiar with this instrument – picture a hollow tree branch about six feet long with a mouthpiece fashioned out of bee’s wax.

The didgeridoo or “didge” is played like a trumpet – the lips are pursed against the mouthpiece and air vibrates them together to produce a long, deep and haunting drone.  Skilful players can control the pitch and overlay shrieks and other sounds.  To play it continuously one needs to employ “circular breathing” to maintain a constant flutter of the lips.

I suggest you listen to this awesome sample of didge from Yanni via Youtube as you read the rest of this post.

I have been passionate about working in Aboriginal Australia for many years. When I was a fourth year Med student ( in the 90s) I entered an essay competition on Aboriginal Health and was lucky enough to win a scholarship elective in rural Namibia.  That summer I spent three months in a tiny town called Keetmanshoop, on the edge of the Kalahari.  I had the fortune to work with some amazingly skilled and battle-hardened doctors in a remote, beautiful and strange world.  If you ever saw the movie “The Gods Must Be Crazy” – then you have an idea.

Namibia, Keetmanshoop in Namaland

Now, my University faculty were keen to thank the Namibian doctors for their generosity in hosting a clueless student.  As such they decided to send a gift, a ceremonial didgeridoo, to the team as a cultural token of thanks.  Of course this meant that I had to carry an eight-foot long, polished tree branch through three borders in order to deliver this gift.

Imagine this scene.  At the tender age of twenty one, I am standing in the Windhoek airport terminal.  The building itself is literally a massive, domed hangar, a single metal room filled with a thousand local travellers.  In my jet-lagged haze I was aware of the fact that mine was one of a few white faces in the crowd queuing at the passport control.   This was the first time in my life that I felt like an “other”, an outsider distinctively different to the crowd.

My passport was stamped and I was asked to present my luggage to the customs officer.  The broad smile of the Namibian official disappeared as I produced a suitcase and what looked like a cannon wrapped in brown paper.  The airport bustle continued around me as he asked me to unveil the contents of my peculiar parcel.  The didgeridoo was completely foreign to this man, he could not conceive of it’s purpose.

“What is this?”

“It is a didgeridoo.”

” Okay…..” he paused, confused. Looking down the lumen for a clue, surely expecting it to be packed with drugs, diamonds or devils.

“It is a musical instrument – you play it.” I explained as he rolled it over like it were a dead snake.

After contemplating my claim for a tense moment, he smiled.

“Okay, man. Play it then.”

I thought he was joking. However, the intense look on his face suggested he was very serious. “Play it!” he insisted.

The desert heat, the crowded queue and the situation had me sweating intensely.  I had raspberried on the domestic vacuum-hose as a kid but this did not fill me with confidence  I knew I could get a note out of it… but would that sound convince this chap of my claims?

I pursed my lips against the now-melting beeswax and took a deep breath.

The long, deep note reverberated all around the huge hall.  A thousand Namibian voices stopped.  The suddenly-silent hangar filled only by my lonely didge drone.  A thousand pairs of eyes now watched as I did my best to convince the officer that this was what a didgeridoo does do.  For what seemed like a long time, but was probably 20 seconds, the room was transfixed by my performance.  The crowd’s response was not applause but laughter.  Hundreds of locals laughed and pointed as my breath expired and the droning didge died. The customs officer could not control his own smile and gave a giggle as he waved me through the gates.  My first hour in Namibia taught me a lot about being an outsider, an “other” and being different.  That moment left a deep imprint in my memory!

That feeling dwells deep in my limbic system.  I use it.  When I see the ancient Aboriginal man in my modern, white ED – my mind goes back to that moment.  I imagine how it must feel to be in a foreign place, where the language is strange, the customs alien and try to be a better human.  Empathy can be deliberate – having walked in the shoes of an outsider for just a few months can give one the skills to practice more inclusively.

That summer in Keetmanshoop was inspirational.  I developed a love of rural and remote medicine.  Living and working in a small community was clearly the best job in the world of medicine.  But that is for another day.  This post is about the didgeridoo – an ancient instrument that just might provide a cure for a very modern disease.

Learning to play the didgeridoo might fix your patient’s (or your own) obstructive sleep apnoea.  Way back in 2006 the BMJ published this paper:

Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial 

This was a Swiss study conducted in Zurich.  Which is pretty much as far from Aboriginal Australia as one can get both geographically and culturally!  Of course the mountain folk do have their own version of the didge, the Swiss horn…swiss horn

Image from the BMJ paper above – Swiss man playing the plastic trial didgeridoo

So what did this trial actually do and what did they find?

This was a randomised controlled trial of just 25 Swiss sleep apnoea patients – so not a massive cohort!  They had OSA but were not yet receiving CPAP or taking any sedatives / excessive alcohol.  They also excluded patients with a BMI > 30 which would exclude a lot of OSA patients I imagine!

The patients were stratified by OSA severity using a few measures (Epworth scale, Pittsburg score, “partner sleep disturbance” and the apnoea-hypopnea index).

They were randomised to either remain on the waitlist for didgeridoo lessons for the 4 months that the trial ran.

The intervention group received didge lessons and instructions to practice for 20 minutes 5 days a week.  Specifically they did learn the circular breathing techniques that involve a lot of upper airway muscle training.  IN the final analysis they actually played on average 6 days a week for 25 minutes… hardcore protocol adherence!

And guess what – it worked!  Well, sort of, it depends on how you measure the success of the intervention.  3 of the 4 measures showed a statistically significant improvement (yes, the all mighty p< 0.05….) Only the Pittsburg score was not significantly altered.

The numbers on the Epworth scale are here:

Now before you all start writing angry comments about the relative weakness of this data… lets remember – this is basically a group of Swiss-German middle-aged men getting together and playing a didgeridoo. I cannot see the downside to this intervention as long as we ignore the auditory insult of their families / neighbours / friends.

I love this trial.  Applying ancient skills to fix a modern problem.  It makes sense to me on a physiological level – stronger pharyngeal and glottic muscles should reduce the airway’s tendency to obstruct.

The cost is basically the cost of a plastic didgeridoo ($94 in this trail).  Of course, they could have just used the family vacuum tube as a cheap, available alternative.

OK, so there you have it.  That is what has been occupying my mind this week.  I actually think I will recommend didge lessons / practice to my patients with OSA symptoms.  Given that I work in the north of Australia -this may be the most culturally-appropriate intervention ever devised for a common problem in Aboriginal health.

Let me hear your thoughts.


First10EM Journal Club: September 2017

Welcome back to another installation of my favourite FOAMed collaboration with Canada’s brightest – the one and only Dr Justin Morgenstern.

This month we will be discussing 9 papers and a few random clinical, curly cases.  As always the full text PDFs of the articles we will be discussing are linked below.  You can also read Justin’s full written analysis of the papers over at Articles of the Month on the Fist10EM blog.

Justin and I would appreciate your feedback on the podcast if you can spare 3 seconds.  We often wonder if we are saying too much, too little or not.  I am also interested in how many folk actually read the articles as part of the Journal club.  Please let us know how you feel about the podcast:

Here is the podcast:

Here are the papers:

Driver BE et al. Flush Rate Oxygen for Emergency Airway Preoxygenation. Annals of emergency medicine. 2017; 69(1):1-6.

Acquisto NM, Bodkin RP, Johnstone C. Medication errors with push dose pressors in the emergency department and intensive care units. The American journal of emergency medicine. 2017

Torres J, Avalos N, Echols L, Mongelluzzo J, Rodriguez RM. Low yield of blood and wound cultures in patients with skin and soft-tissue infections. The American journal of emergency medicine. 2017; 35(8):1159-1161.

Chiang E, Bee C, Harris GJ, Wells TS. Does delayed repair of eyelid lacerations compromise outcome? The American journal of emergency medicine. 2017.

Millin MG, Comer AC, Nable JV. Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis. Resuscitation. 2016; 108:54-60.

Lauria MJ, Gallo IA, Rush S, Brooks J, Spiegel R, Weingart SD. Psychological Skills to Improve Emergency Care Providers’ Performance Under Stress. Annals of emergency medicine. 2017.

Steele DW, Adam GP, Di M, Halladay CH, Balk EM, Trikalinos TA. Effectiveness of Tympanostomy Tubes for Otitis Media: A Meta-analysis. Pediatrics. 2017; 139(6).

Roberts JR, Dollard D. Alcohol levels do not accurately predict physical or mental impairment in ethanol-tolerant subjects: relevance to emergency medicine and dram shop laws. Journal of medical toxicology. 2010; 6(4):438-42.

Ramirez R, Stalcup P, Croft B, Darracq MA. Haloperidol undermining gastroparesis symptoms (HUGS) in the emergency department. The American journal of emergency medicine. 2017; 35(8):1118-1120.


A COMPASS that points Nor’west

Today I’m on a deep dive into a newly released trial that has the potential to change the way we manage chronic, stable atherosclerotic disease.  The trial under the spotlight is the COMPASS trial (full text PDF here) published online in the NEJM on August 27, 2017.  It was launched at the European Cardiology Society (ESC) meeting.

COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) is a massive three-armed randomised, double-dummy placebo controlled trial looking at three different anticoagulation strategies for patients with “stable atherosclerotic disease.”  In total more than 27,000 people were recruited.  The trial took place in 602 recruitment centres in 33 countries which included patients from all continents.

The trial is still ongoing as it involved 2 separate trials – one looking at the three anticoagulation strategies which has now been published; and another looking at the effects of pantoprazole on bleeding outcomes (still in process).  The current published article is the result of the anticoagulation part of COMPASS being stopped early due to interim analysis observing a benefit in the combination arm in February 2017.  This grabbed a bit of media attention and even got headlines in the mainstream media (see Reuters article).  More on this later.

It should be stated that this trial was sponsored by Bayer who produce both rivaroxaban and pantoprazole. The market for these agents would be greatly expanded if it were found that they conferred a benefit to such a common indication as “stable atherosclerotic vascular disease.”  This is high stakes stuff!

I am going to ignore the ongoing pantoprazole trial for simplicity.  I will also largely skim over the 3rd anticoagulation arm (rivaroxaban 5mg bd only) as it did not really get a guernsey.  The easiest way to analyse this trial is as a comparison of aspirin 100mg EC + placebo vs. aspirin + rivaroxaban 2.5mg bd. 

So lets describe the trial using the PICO template and later I will delve deeper into some of the hazy details.


As stated this was a big, international trial.  The majority were “Western white” folk. About 38% were non-white, mainly from Asian countries.  The average age was 68 years and about 78% were men.

They were typical of the type of patients we envisage when we think of vasculopaths – hypertensive, some smokers, diabetics… all the usual suspects.  90% of the patients had coronary vessel disease and 27% had peripheral vessels disease (so 17% had both).  As one would expect -they took a lot of the medications we love to prescribe ACE-I, CCBs, statins, diuretics and B-blockers.  The beauty of such a large trial is that there is no baseline difference in any of the groups’ profiles.

The inclusion criteria seem fair enough to me – the patients needed to have documented coronary or peripheral vessel disease and those who had coronary disease only and were under 65 years old needed to have 2 other risk factors or documented disease of 2 separate vascular beds.  These are the folk we would all usually prescribe aspirin for secondary prevention as per every guideline out there.

The study included 1448 patients who had undergone CABG (bypass surgery) and went straight onto be randomised.  For me this seems like an odd inclusion as this group clearly has specific risks and does not really reflect the patients we are seeing in outpatient care and deciding how to manage. I would think that group should be analysed separately… but I could find no way to break this down in the data provided.

The exclusion criteria are vital to understand – we need to know who was not in the study so that we can understand he outcomes and know to whom we can apply the evidence  in our own practice.  Many of these are straightforward exclusion criteria. However there are a few you need to know about:

  1. High risk of bleeding [not really further defined… unclear if a score or decision-aid was applied]
  2. Stroke within 1 month or any history of hemorrhagic or lacunar stroke
  3. Severe heart failure with known ejection fraction <30% or New York Heart Association (NYHA) class III or IV
  4. Estimated glomerular filtration rate <15 mL/min
  5. Any known hepatic disease associated with coagulopathy

These exclusion criteria would remove a good proportion of my patients from the trial.  So be aware of this before reaching for the script pad!

This trial also employed a “run-in period” where patients were given aspirin + placebo rivaroxaban for a period and reviewed for adherence, side effects and adverse effects.  In this paper 1645 (nearly 6%) were excluded for ‘adherence concerns’.  I find this problematic.  This seems to create an idealised population which is divorced from the reality of our daily practice.  It would be great to know about the side effects, non-compliance etc in advance….  but that is no how medicine works!  I suspect that the use of a “run-in” phase will remove some patients who we would struggle with in the real world, enhance the Hawthorne effect and may improve the performance of the intervention artificially.


The anticoagulation strategies on trial were 3:

  1. Aspirin [enteric coated 100 mg] alone
  2. Rivaroxaban 5 mg bd alone
  3. Combination of aspirin 100 mg + rivaroxaban 2.5 mg bd


The use of aspirin is really the gold standard in secondary prevention – and as such this would be considered the control group.


The primary outcome was a composite one [not sure why, it makes for tough analysis]. It was one of:                      – cardiovascular death, stroke, or myocardial infarction.   Each of these was defined by valid measures.

(Note the primary outcome was NOT “all cause mortality” which we do bang on a lot about here on the blog… it is probably the best measure of such an intervention given the balance of risks and harms.

The secondary outcomes were a couple of other mixed/ composite somewhat overlapping outcomes: –

  1. the composite of ischemic stroke, myocardial infarction, acute limb ischemia, or death from coronary heart disease;
  2. the composite of ischemic stroke, myocardial infarction, acute limb ischemia, or cardiovascular death;
  3. and death from any cause.

The measure of safety / harm was defined as  the International Society on Thrombosis and Haemostasis (ISTH) criteria for major bleeding and included fatal bleeding, symptomatic bleeding into a critical organ, bleeding into a surgical site requiring re-operation,or representation to an acute care facility.

Here is the main efficacy outcomes from the trial:





As you can see – there was no real statistical difference between the aspirin alone vs. the rivaroxaban 5mg bd groups.  All of the confidence intervals cross or scrape 1.0.  So I will focus the rest of the analysis on the comparison between the aspirin alone vs. rivaroxaban + aspirin groups.

There was a significant difference between the groups favouring the combination when we look at the primary outcome and the other composite end points.  So that looks good.

Now what about the downsides – the bleeding?  This was also presented in the paper with a “Nett clinical benefit calculated which attempts to weight the absolute benefits against the bleeding risks.  Of course, it is hard to do this as an absolute comparison as we are not comparing apples with apples – it is not a bleeding death cancelling out a life-saved by the intervention.  So although it is a neat way to look at the risk : benefit, I am not convinced.  This system is prone to definition creep and may not really reflect the patients’ values.  If you prefer your stats simple you could summarise COMPASS as follows:  “There was a 1.3% benefit over a 1.2% risk of bad bleeding…”

Table here:







The primary outcome occurred in 1323 patients of the 27,395 who completed run-in and were randomised.  This is 4.8%.  However, the power calculation was based on a total of 2200 primary events, which was estimated to need 27,400 enrollees.  So it appears that the total number of patients enrolled was very close to the magic power calculation requirements…. but, the number of events falls way short by nearly 900 “primary events” due to a lower than predicted event rate. It is important to appreciate this distinction in an event-driven trial.  To get enough events they would have needed to recruit about 45,500 patients to achieve the power set out in the original calculations.


The COMPASS trial was halted prematurely after an interim analysis by it data monitoring board found the benefit of the combination therapy crossed the predetermined life of significance.  This decision was in keeping with the rules laid out in the trial protocol.  But what does early stopping do to the outcomes?

Early stopping has the effect of overestimating the benefit of the intervention.  This is especially true of smaller trials, however even in large trials like COMPASS it can have a significant effect.  There are many examples of clinical trials which have been stopped early and then subsequent data from other sources have shown the benefits to be small or non-existent.

The other harm that can come from early-stopping is the subsequent difficulty in carrying out a subsequent trial which may confirm or refute the hypothesis being tested.

So what does this mean?  It is a tricky ethical area for clinical researchers.  I think for COMPASS it means that we should be cautious with our adoption of it s findings.  The most likely effect is a small overestimate of benefits of the combination therapy – and given the small benefit over risk –  this could be enough to land us at equipoise.


About half of the benefit seen with the combination therapy over aspirin alone was due to the reduction in ischemic CVAs.   Now if you scour the fine print you will discover that only 1.3% of the patients in the trials were found to have AF as a comorbidity.  This does seem low in a cohort of vaculopaths aged in the 60s.  In a recent Australian survey the baseline rate of AF in men > 55 years was closer to 6%.

SO we may have a problem here.  If the AF was ‘occult’ then we are looking at a cohort who have AF, are at risk of CVA and therefore would more likely benefit from a more aggressive anticoagulation strategy.  A proportion of the benefit seen in the COMPASS trial may have evaporated if we excluded folk with AF as we deemed them to be in need of more than “just aspirin” at the outset.


The Forest plots presented in the Supplementary appendixes show an interecting finding which is kinda intuitive when you think about it.  Specifically if we look at the risk and benefits broken down by age-strata….. here:



As you can see – if you break the numbers down by age groups – < 65, 65-74 and > 75 a clear pattern emerges.  The benefits gets smaller to the point of non-significance as one gets older and the risk of major bleeding goes up to double once you are over 75.  So that delicate balance between good and bad is tilted by the march of time.  It may be that there is a benefit to the combination in younger folk which tilts to a nett harm after 70-odd years.

This makes complete sense in my mind and I think we need to keep this in mind when applying this data in the real world.


The COMPASS trial is big.  Your local friendly Cardiologist / Physician / Hospital or Vascular Surgeon will likely be getting bombarded with media releases, pharmacy reps and guidelines based upon this trial in the near future.  As GPs we are in the unique position of having to counsel, monitor and tweak our patients medications to suit their needs over the long term.  This trial will spur a push towards more aggressive anticoagulation combinations in those patients we previously plied with simple willow bark extract!  We need to know what the data actually says about the risks and benefits of these more aggressive combinations.

To my mind the benefits and harms are closely balanced. Maybe towards benefit in younger folk, harm in older people.  There are a few big issues I have with the trial such as the early stopping, the choice of outcomes and the large drop out due to “run-in failure”.  I for one, am not sold just yet.

Unfortunately I do not imagine this question being re-examined on such a scale anytime soon.  We need to need to know what this data really says, look past the headlines and help our patient’s decide what risks they are prepared to accept for some small gains.

Please have a read of the trial, look at the raw numbers and make up your own mind.