No Xray, No Problem: the evidence

So in case you missed #SMACC in Chicago – I was lucky enough to be able to talk about one of my greatest passions – bedside Ultrasound.

The talk was a bit of the evangelical side – the goal being to try and make the audience think about how we image patients. I wanted to show how I use US to be faster, better, more effective and safer in delivering care.  I deliberately tried to avoid a long-winded evidence  discussion.  After all – it is SMACC, entertainment is important too!

You can pop over to the Intensive Care Network or to the SMACC website to check out the audio and slides from the talk.

So here is the evidence – the references for my talk.  You could also go back and look at this post “Bedside US Evidence Echoes” and the fascinating discussion of ultrasound evidence in the comments thread.

Lets start with the trauma case:

Colle’s fracture diagnosis and reduction:

How to find the axillary brachial plexus from Mike Stone on Vimeo.

Paediatric PUO ie. “Pyrexia that’s Ultrasonographically Obvious”

Sepsis Resuscitation

Bowel Obstruction

Neonatal Lung Ultrasound


Happy scanning

& remember ultrasound gel is the lubricant to smooth the patient’s journey through the ED!


Own the Patient (Clinical Case 126)

It is January – so in Australia that means it is the time of year when all of the junior doctors in the country rotate into new jobs, hospitals and towns.  Here in Broome we have taken on a brand new cohort of super-smart residents [and welcomed back some old faces].

Inspired by some discussions I have had with fellow educators online and in person I have decided to try something a little different this year.  We will still be rolling out the same “regular” medical education, sim training and bedside / floor teaching. However, I am promoting a new concept [not really new, just formalised].  I call it “Own the Patient”.

One of the things I love about my job is the way our place is structured.  As a generalist in the hospital I have the opportunity to treat a patient “from door to discharge”.  I can meet them in triage, admit them, take them to theatre for an anaesthetic, arrange their recovery and care for them on the ward afterwards.  Our trainees on the other hand are constrained by their roles – the ED RMO admits, the Surg RMO assists etc….

This is tradition – it is how we do business and it works. But….  there is a lost opportunity.  I believe that much of what I have learned over the years, especially many of the subtleties and nuances of medicine, have come from following my patients through their inpatient journey.

Closing the loop on your emergency care by following your patient through their care is a potent learning habit.  Most of us are good at following up our “interesting” or “difficult” cases.  Rarely though do we make the effort to check-in on the 76 y.o. chap with a mild exacerbation of his COPD.  Patients have so much to teach us – and yet we routinely decline the offer of free tuition.

So – I hear you thinking: “That’s all very nice, but how will we actually harness this educational trove?”  Let me explain:

Here is the current state-of-play in most places I have worked.  The ED docs admit the patients, and those with “interesting” diseases, symptoms etc are followed by stealth almost.  We check their bloods and images on the computers.  We might call up the inpatient team to see what happened to them or chase the surgical pathology.  Rarely do we actually go to the bedside and visit our patients.

So here is the plan, the instructions to how one might “Own the Patient”.

  • At some stage in each shift our ED residents will be encouraged to “visit” their patients on the wards.
  • Ten or fifteen minutes during the inevitable lulls.
  • I want them to specifically visit the “standard” patients, e.g.  the ‘mild COPD’ or the ‘RUQ pain for investigation.’
  • When I say “visit”, that is exactly what I mean.  I want them to go to the bedside in the same way a concerned relative might do.
  • They should not check on the progress with their inpatient colleagues first – I want them to go in and get an untarnished patient perspective.
  • When they visit the patient whom they admitted I want them to ask 3 simple questions:
    1. How are the symptoms that lead to their ED presentation going?  Have they been relieved?
    2. Ask them to explain what has happened since admission – ask the patient to explain their understanding of what has happened to them OR what do they understand the treatment plan is going forward.
    3. Ask, “is there anything I can do for you?”
  • After visiting they can then go and do all the usual doctorly things – look at the CT, chase the bloods or get the 30 second thumbnail from the inpatient team.
  • As they walk back to ED I want them to meditate on what they could have done differently to make that patient’s experience easier, less painful or less confusing.

(Addit:  A few astute commenters have noted the potential for this “visit” to lead to conflict on the wards…  here is how I imagine it will play out.)

  • Most of the patients will be pleasantly surprised that their ED doc took the time to come visit and be uncomplaining.
  • The ED RMO will almost always notice a few things that they could improve upon for future patients – the 1%-ers, of “no clinical importance”.
  • Sometimes the futility of admission will become apparent – could we have done the same or better as an outpatient?
  • Sometimes there will be an opportunity to provide some simple education and decrypt some patient confusion (e.g.. why did that nurse need to give me the blood thinning injection – I thought  had a chest infection not a clot….”
  • Occasionally the visit will reveal either serious missed information or potentially useful data – this should be formally noted and brought to the treating team’s attention – in the same way that the night ward cover MO would not “take over care” but ensure that appropriate immediate action was in place and communicate it to the admitting team.
  • I really hope that this may actually breakdown some of the “Us vs. them” tribalism that take place in hospitals.

Hope that last step – the team feedback makes sense to you all.


This exercise is hopefully going to allow the residents to get a fresh and realistic perspective on what patients go through after we take the decision to admit.  A chance to understand the peculiar rituals of wards, the confusing language, the disempowerment of being in “a bed” tied to drips and lines.  This is what I want them to learn.

Here is an anecdote to illustrate the point I am making.  This really happened just last week when I went to visit a lady on my own “Own the patient round”.

Helen is a 68 y.o. Aboriginal woman who lives in a community a few hours out of Broome.  She was raised in a mission, never drank alcohol in her life and is pretty shy.  English is her second / third language.  She has type 2 diabetes, chronic renal failure and COPD all of which are well managed by the local community clinic.  She gave up smoking last year after her sister had an nasty STEMI.

Helen developed a flu-like illness a few days prior and was being treated with salbutamol and a course of prednisolone at home for increasing wheeze and dyspnoea. She was transferred down by road [2 hours drive on a rough gravel track] as she was not improving and has a history of needing oxygen when she gets crook.

On arrival she was moderately dyspneic, sats 92% on nasal prong O2 and RR = 28/min.  She was still wheezy.  We did all the usual things.  She got some antibiotics and bloods done – which showed a deterioration in her renal function.  This was probably due to being a bit dry and her BSL was high (23 mmol/l, ~ 414 mg in the USA)  as a result of the infection and steroids.  In Broome we use a basal bolus insulin regime to control our inpatients’ hyperglycaemia – so she was started on SC insulin ‘as per protocol’.

The medical plan was to keep up the bronchodilators, keep the BSL around 10 if possible and give some IV hydration overnight to get the beans flowing.  Easy really.

So 16 hours later I popped up to see Helen. She was not looking too well.  She was tired, worried and keen to get out of hospital ASAP.  The breathing was a bit better with the oxygen and inhaled meds – but she was still chugging away.  She had not been up and walked or sat out of bed as she was too tired.

When I asked how she was going she told me that she was very thirsty, tired and that her left arm was “stiff”.  Odd.

When I pushed her to explain she told me that her arm was stiff as she had been holding it out straight all night.  The IV in her arm was “tricky” – if she bent her elbow the pump kept beeping and waking up the other 3 ladies in the room.  She had fallen asleep a few times but was woken once when the alarm “boinged” and once when the nurse came in to admonish one of her room-mates for trying to climb out of bed as she was a “Falls Risk”.  She didn’t sleep much after that… she was related to old lady in the next bed and was worried for her.

Helen had not passed much urine.  She felt thirsty but the water jug was on the same side as her drip arm and she was too shy (scared) to ask the nurse for help or to get out of bed and move it.  Because of the pump trouble she had only received about half a litre of the prescribed fluid via her veins.

I asked about the medical plan – and she was upset about the insulin.  She knew about the needles.  She had discussed them with her GP, but was reluctant to use long-term insulin.  Her sister had been on it – and put on weight.  Then she had the heart attack.  It was not a good medicine in Helen’s mind.

When I asked Helen if there was anything I could do for her.  She smiled. “Can you pass me that water please?”

I went back to the nurses station and read the notes.  The medicine was spot on.  Moderate COPD, maybe viral.  Hyperglycaemia and bump in renal function, poor urine output overnight.

The medication chart was interesting – where the insulin was prescribed the nurses had drawn an “R” for patient refused.  On the back was prescribed nocte temazepam for insomnia.  Two more litres of IV fluid had been ordered.  The nurses had noted the IV was “positional” but functioning OK for IV antibiotics.

Her CXR looked normal, but her creatinine has risen further.  Her BSLs remained in the 20s.

For me this was a fail.  It was not a medical error, or lack of knowledge.  This was a failing to do a few simple things well.  I call them “the 1%ers” – it’s an Aussie football term.  If we do the little things well, apply a fraction more effort then the big picture can work out much better.  This is not the stuff of heroics.

What would I do differently after visiting with Helen?

  • I would have checked that the IV was working, that she could move her arm freely.
  • I could have resited that drip to a better spot.
  • I could have communicated the importance of oral hydration to the ward team more explicitly
  • I should have spent time explaining why I wanted to use the short-term insulin
  • I could have explored her fears around insulin and reassured her it was just for a few days.

These outcomes will never be counted in audits, but they matter.  The only way to learn the 1-percenters is to close the loop.  Go and talk to your patients.  Understand their experiences and then try to do better.  This stuff is largely tacit learning – it is unteachable.  One must consciously try to experience the “little” problems in order to prevent them from recurring.

So that is why I want to have a crack at “Own the Patient”.  We train very smart young doctors and yet we still have problems in healthcare.  Maybe this is one way we can guard against unnecessary suffering and make our patients experience  that little bit better?

Let me hear your thoughts.



Clinical Case 125: Tricky Trauma Tachy

Hello team,

I have a really special treat for you all. Drum roll…..  A brand new guest contributor here on the Broome Docs blog!

Today’s case comes from one of my favourite FOAM folk – Dr Victoria Stephen.  In case you have not met or followed Tori  – stop what you are doing and jump onto her Twitter feed – @EMcardiac .  She is my personal FOAM superhero – she works in one of the biggest, busiest and craziest hospitals in South Africa and loves to use the Ultrasound as much as I do!  Incredibly humble & understated, Dr Stephen ‘walks the walk’ of which we hear so much talk about in the FOAM community.

So now – lets get onto the case.  This is a trauma case.  Imagine you are working in a really busy trauma ED in the bad part of Johannesburg.  Stabbings, shootings and MVAs are rolling in all day.  Your ED is stretched to the rafters with patients needing your care…  in rolls the next patient.

A 33 year old pedestrian was brought to the ED by EMS. He has been hit by a car. The paramedics report that he is haemodynamically stable and alert with a suspected left femur fracture. A trac-3 splint is in place. A lodox scan is done in resus while he is still on the spine board and this is what it shows:

A lodox scan is a low dose radiation X-ray machine which is capable of producing a full body X-ray within 15 seconds. It is located at the entrance of the resuscitation room and is useful as a screening tool in trauma patients to rapidly detect major fractures and potentially life threatening injuries.

A lodox scan is a low dose radiation X-ray machine which is capable of producing a full body X-ray within 15 seconds. It is located at the entrance of the resuscitation room and is useful as a screening tool in trauma patients to rapidly detect major fractures and potentially life threatening injuries.

 There is clearly a femur fracture on the left.  How is his pelvis?

Zooming in on the image: There are no major pelvic fractures. A left sided midshaft femur fracture is present. A trac-3 traction splint is in place.

Zooming in on the image: There are no major pelvic fractures. A left sided midshaft femur fracture is present. A trac-3 traction splint is in place.

A minute later he is placed onto the resus stretcher. The patient is restless and complains of severe pain in his left thigh. He is rather pale and diaphoretic. Monitors are placed, recording a heart rate of 180-185 BPM, and the automated BP machine is having trouble recording his blood pressure. The patient does not appear as stable as previously thought. He feels cold to touch and his radial pulses are not palpable. A second large bore line is placed, fluids are started and blood is sent for crossmatch and blood gas analysis.

While the treatment is begun, a search for the cause of shock is underway. As ATLS teaches, the top three causes of shock in the trauma patient is haemorrhage, haemorrhage and…haemorrhage. So an eFAST is performed, and is negative. . There is no external blood loss from head wounds or anywhere else. The femur is already well splinted. A pelvic fracture is considered but the lodox scan has already shown that there are no pelvic or other extremity fractures. The mediastinum does not look wide and no pneumothorax is present. The blood gas comes back: pH of 7.32 pCO2 30 mmHG, Hb 12.0 g/dL and BE -10. After a litre and a half of crystalloid, his BP is 80/50, but the heart rate hasn’t shifted, racing away at 180-190 BPM.

A repeat eFAST is still negative. His BP is 100/65 now, but keeps dipping down to 80/50. Blood is being crossmatched, just in case, although a repeat blood gas looks much better. Despite this, the patient appears to be a transient responder to resuscitation. What could be going on?

Haemorrhage is still a possibility, particularly into the retroperitoneum. An eFAST is notoriously poor at making this diagnosis, and he’s just not stable enough for a panscan at the moment. The CT scanner is a fair distance away.

The patient may just be inadequately resuscitated. This may occur particularly in crush injuries and severe burns, if resuscitation is delayed or if the patient presents late. However this is unlikely in this case.

Another form of shock could be present. Obstructive forms of shock such as tension pneumothorax and cardiac tamponade have already been ruled out. Neurogenic is unlikely as he has no disability / evidence of thoracolumbar or neck trauma.  This degree of tachycardia is pretty unusual for an adult. It also has not changed at all despite fluid resuscitation. One can’t make out the p waves on the monitor, either. A 12-lead ECG is done:

What does it show?

What does it show? No P waves are visible. A regular narrow complex tachycardia @ ~ 180/min is present, most likely an AVNRT.

A myocardial contusion from blunt chest trauma is a good consideration. Dysrhythmias commonly occur as a result and most often manifest as sinus tachycardia, atrial fibrillation or ectopic beats. The patient denies any chest pain and no chest trauma is visible.

Thinking beyond trauma, recreational drugs and underlying illnesses should always be considered. He denies taking any recreational drugs; has no known medical conditions and denies having any palpitations. He was completely well until he hit the fender of that car.

Regardless of the cause or precipitant of the SVT, it requires treatment. Valsalva manoeuvres are attempted in the form of blowing a syringe and carotid sinus massage, but aren’t successful. Adenosine 6mg is given, which is followed by the seemingly eternal sinus pause. A sinus rhythm at 80 BPM commences thereafter and he remains in sinus. A 12 lead ECG done:

The patient is in sinus rhythm. The PR interval is approximately 120 ms, but there are no other features to suggest a pre-excitation syndrome.  As noted - the BP is now 101/63...Casey: Recent blogpost on using CCB for SVT – this is clearly one situation where it would not be a great idea.  Rare combination of events.  This is where the protocols go out the window and you need to have a group huddle and think on the fly.  Medicine – still an art, despite all the science!

The echocardiogram and CT angiogram of the chest are normal. Serial troponins are negative. He is transferred to orthopaedics after 24 hours of observation in high care and has an uneventful hospital course. He is referred to the cardiology clinic for further electrophysiological studies.

Casey: Now that is a really fascinating case.  Dr Stephen and I had Twitter discussion about the medicine and the cognitive errors that cases like this bring to the fore.

So, let’s perform a further cognitive autopsy:

System 1 thinking is the rapid, intuitive form of thinking that relies on pattern recognition. It often serves us well, particularly in trauma resuscitation, where diagnosis and management often need to occur simultaneously. System 2 thinking which is slow, deliberate and analytical reasoning may not appear to have a place in the trauma resus bay, but is proven to be more accurate than system 1 when dealing with more obscure presentations. Surprisingly, even in a trauma resus, we have more time to think than we perceive. Particularly in unusual presentations, a cognitive checkpoint should take place where the team pauses to consider whether anything has been missed or not been considered.

Pattern recognition can be useful in leading to a rapid diagnosis but it can lead to anchoring bias, where an initial diagnosis is focused on at the expense of other diagnoses not being considered. In this case, where shock was recognised, it made perfect sense to begin treating and investigating for the most common cause of shock in trauma – haemorrhage. But the heart rate was too high and out of keeping of other clinical findings, such as the patient’s improving blood gas and perfusion. Another form of shock was present. System 1 thinking will prompt one to recall a familiar, common diagnosis first. In a dedicated trauma unit, an SVT was a foreign entity, so was not initially considered.

How can we improve our thinking in trauma resuscitation and reduce cognitive error?

  • System 1 and 2 thinking both require a solid knowledge base to avoid error. Courses with intense training in trauma are a good start. There is no substitute for knowledge, training and experience.
  • Be aware of cognitive biases in the trauma setting. Search satisficing, which is stopping to look for other injuries or conditions after one particular injury is found, is common. Examples include failing to look for more than one fracture after the first fracture is found or failing to recognise the potential of occult bleeding in the patient with neurogenic shock from a devastating spinal cord injury.
  • Situational awareness as applied to the medical field is described as “the detection and interpretation of situational clues from multiple, dynamically changing sources (including from patients, other members of the team, and from displays and equipment), thinking about what might happen in the future and adapting to evolving situations”. Situational awareness is improved by the use of a Trauma Team leader to guide the overall resuscitation while other members are focused on critical tasks. Other strategies to promote situational awareness in resus teams to reduce medical error such as simulation, shared mental models are well described in this paper: “Beyond crisis resource management: new frontiers in human factors training for acute care medicine” by Andrew Petrosoniak and Chris Hicks.
  • Performing a tertiary survey once the patient has been stabilised and life threatening injuries have been managed. This includes a head-to-toe examination looking for potential missed injuries such as a scaphoid fracture. It also may include further enquiry into the patient’s past medical history and consultation with other specialists as appropriate.

Patients often fail to read the medical textbook. It’s up to us to recognise unusual presentations, adapt our thinking and improve patient safety.

Interested to read / hear more on the cognitive side of what we do? Check out these links as a starter.

Pitfalls in the evaluation and resuscitation of the trauma patient. Mackersie RC. Emerg Med Clin North Am. 2010 Feb;28(1):1-27, vii 

From mindless to mindful practice – cognitive bias and clinical decision making. Crosskerry P. N Engl J Med. 2013 Jun 27;368(26):2445-8 

Beyond crisis resource management: new frontiers in human factors training for acute care medicine. Petrosoniak A, Hicks CM. Curr Opin Anaesthesiol 2013 Dec;26(6);669-706 

Exploring situational awareness in diagnostic errors in primary care. Singh et al. BMJ Qual Saf 2012 Jan;21(1):30-8

Achieving quality in clinical decision making: cognitive strategies and detection of bias. Crosskerry P. Acad Emerg Med 2002 Nov;9(11):1184-1203 

Ed:  Of course if you like your cognitive psychology delivered in the theme of Star Trek by a cheeky, dimpled Intensivist then you should go back and see this talk from the original SMACC conference in Sydney 2013…  “All Doctors are Jackasses” by Chris Nickson.


Thanks to Tori for sharing this case and the cognitive autopsy.  These are exactly the types of cases where things can go wrong despite all the right moves.  Sometimes we just need to think better – this is hard to do in the moment, but awareness and the discipline to stop and rethink are key in my opinion.

If you would like to hear more from my favourite African Doc then please let me know… I reckon we can twist her arm to do a few more?



Clinical Case 124: Sand, Surf and Shattered Shin

Today’s case is maybe not unique to Broome.  Representative of every Aussie town where teenagers, cars and boredom seem to intermingle to create crazy injuries… and sadly; occasionally tragic deaths.

Our 24 yo lad [almost always a male] presents to the ED with a bunch of his mates in the back of a ute [never a good sign].  They all seem very merry, aside from our hero.

He was “bonnet surfing”: a pastime in which an old car bonnet is inverted, tied to a length of rope and dragged behind a car on a beach / paddock / road.  The aim of the game is for the young man to stay aboard the said bonnet whilst his mates try to dislodge him by driving it over obstacles such as tree stumps, sand dunes or edge markers….  genius!

The story: he was doing well until he hit a bump, flew in the air and his shin collided with a metal pole that was poking out of the ground.  They estimate he was going about 45 km/hr when he hit.  He did not hit his head and was able to stand on one leg… although the other leg is “munted” as we say in Oz.

Gustilo type 2 fracture

Case courtesy of Dr Mansoor Ahmed, <a href=""></a>. From the case <a href="">rID: 12959</a>

Case courtesy of Dr Mansoor Ahmed,, rID: 12959

So – here we are.  We work about 1000 miles from the closest Orthopaedic services.  This guy has a wound with bone and marrow on view.  The wound is filled with sand and little bits of debris from the beach.  As you are drawing up the ketamine to facilitate further inspection and immobilisation you are imagining the long days he will spend in a hospital somewhere fighting off infection, hoping his bones will heal and that the skin will survive.  This is a nasty injury- one that could result in serious disability.

Earlier in the day you flew a STEMI patient south and evacuated a sick neonate to the east… so all of the planes are in the air.  There is going to be a long wait to get our man to somewhere that he can get his leg fixed.

He needs a washout and debridement ASAP.  We have the ability to give him an anaesthetic and get the job started.  So what exactly should we do?

Most big hospitals use all sorts of fancy irrigation systems, high-pressure pulse guns etc. Of course, we do not have these.  So what is the best option in the bush for doing the best washout possible and hopefully allowing the wound every chance to get clean.

This is an interesting clinical scenario for me as we have always “done our best” in the bush with these sorts of injuries.  I have always thought that we were doing OK, but felt that our capacity to do “best care” was limited by the kit we have available.  So I was very interested to read this article in the New England Journal last week.

A Trial of Wound Irrigation in the Initial Management of Open Fracture Wounds: the FLOW Investigators. Dec  31 2015. NEJM

Lets PICO this one.

POPULATION: This was a big trial (by Orthopaedic standards) which randomised over 2500 patients to a 3 x 2 design.  They were patients from 41 hospitals in Canada, USA, India, Australia and Norway.  They had a variety of fractures and severities.  About 2/3 had lower limb fractures and there was an even spread over severity grades – 37% were Gustilo grade II – like our man.
An interim analysis resulted in an expansion of the number of patients recruited in order to cope with follow-up failure which was about 10%.

The INTERVENTIONS consisted of 2 different irrigation solutions [delivered by one of 3 pressure kits]:

  1. Normal saline
  2. a 0.45% solution of castile soap in normal saline

and 3 different pressure set ups [using the 2 different solutions].

  1. very low: gravity
  2. low pressure : 5 – 10 psi
  3. high pressure: > 20 psi

There was a very high level of adherence to the protocol (96.5% – 98.8%) on the initial washout, however this did decrease to about 75% on the subsequent interventions.

CONTROLS There was obviously no “placebo”- so each group acted as controls.  Washouts occurred on average about 9 hours after injury with good consistency across the groups.  The analysis was stratified by injury severity to compare apples with mashed apples. All the other demographics aligned well across groups.

OUTCOMES    The primary end-point was “reoperation within 12 months after the index surgery for promotion of wound or bone healing or treatment of a wound infection.” This is an interesting one as it can cut both ways – inadequate washout may lead to more infections and revisit to theatre, whereas aggressive washout was thought to interfere with healing, may cause tissue damage and subsequent healing problems.  But I think this is a good patient-oriented outcome as it reflects the things we care about – the need to do more interventions for whatever the reason.

As secondary endpoints: non-operatively managed infection and wound-healing and bone-healing problems within 12 months after the index surgery.  These were all predefined and seem like reasonable things to count in this sort of trial.

They used a Cox regression analysis which is the flavour for these longer term outcome trials.


When we look at the various Pressure of irrigation – very low, vs low vs high…  NO DIFFERENCE.  So it did not seem that the pressure of the kit used made any difference to these outcomes.

When looking at the irrigant used – saline vs soap in saline there was a difference seen.  The plain saline group came out better than the soap group 11.6 vs 14.8 % needing a repeat procedure – so a number needed to harm (or benefit) of about 31.

Subgroup analysis suggested the harm was mostly seen in terms of malunion requiring implant exchange surgery.  So a bone healing problem – of course this is a subgroup, so don’t quote it aloud!


The authors discussed a number of subanalyses – looking at various fracture sites and antibiotic usage etc.  Not much to say about any of that though there was a trend to better outcomes for tibial fractures [like our patient] using very low pressure and straight saline.

For me this is one of those papers that helps us as rural / remote and under-resourced providers feel good about what we are able to do in our smaller centres.

Our patient can go to theatre and have a generous washout using 6 litres of saline with low-pressure irrigation and we are doing as well as we can.. and are practicing best care.  Sure- he is still going to have 24 hours delay to getting his ORIF done – but he doesn’t need to wait for a good washout.

Love it.

Let me hear your thoughts.

Broomedocs in 2016


Welcome to Broome Docs in 2016.

Yes – it is that time of year where we look back at what has happened and try to decide on how we might do it better on this lap of the Solar circuit.  I am not one for big “New Years resolutions” so I will not be making any here.  I am going to let you all know a little about what is happening ‘behind the scenes’ in the Broome Docs studio.  There are a few new things, more of the old and some stuff that I am hoping will make your job just that little bit easier.

First, an apology.  It has been a slow semester on the blog and the podcast.  This is the result of a lot of factors – family, fun and future projects.  I have made a decision to focus my efforts on a few “high quality / longer term” projects this last 6 months.  This has inevitably meant that there are less hours in the day to produce the sort of content that you have become familiar with here on the site.  I plan to keep putting up cases, podcasts and editorial stuff as often as I can.  So what is happening in the backstage area?

Primary Care RAP

A year or so ago I joined forces with a gang of Primary Care doctors from all over the USA & Canada.  We have been creating the Primary Care RAP podcast out of the HippoEd studios which famously produces EM:RAP, Peds RAP and a few other quality Med Ed podcasts.  This is not FOAMed – you have to subscribe and pay for the content.  I reckon the price is well worth it.  You get 3 hours a month of Edutainment – high quality, up-to-date, well presented education.  It is narrated by my mate Dr Rob Orman of ERCast.  There are usually about a dozen 10 – 20 minute chapters each month which cover the whole gamut of primary care.  There is a heap of article reviews and we do our best to take all that evidence, boil it down and feed it to you in a fun and digestible format.

A lot of the stuff I write about or rant about on the podcast gets “reborn” over on the PC RAP podcast.  So if you are missing the podcast a bit and need to fill your commute to work – then do yourself a favour and try it out.

SMACC Dublin

Yay! Its on again – the finest medical conference on the planet.  The 4th SMACC is going to be held in DUBLIN, Ireland in June 2016.  I am really looking forward to heading back to the emerald Isle.  I was last there as an elective exchange student in 1998 – and had a blast.  This year I will be trying to top my previous efforts with a lecture, 2 workshops a bit of Tweeting and hopefully another epic musical parody.

SMACC is a huge event and the bar is set very high.  My topic this year is “Diagnosis” which is somewhat broad!  I am hoping to bring a bit of GP commonsense to the modern medicine as it goes in the high-tech, fast-paced critical care world.  Tim Leeuwenberg has been banging on for a while now about how we should be doing better with our GP conferences.  I have learned a lot about presentation skills over the last 4 SMACCs – and I will be dedicating dozens of hours to this one.

Introduction to Bedside Ultrasound

A few years ago Matt & Mike from the Ultrasound Podcast called in a bunch of US nuts from all over the planet to create a ground-breaking textbook.  The Introduction to Bedside Ultrasound  was a huge success which flew off the electronic “shelves”.  The lads were in a position to make it free – awesome.  This is why I love the FOAMed crew – they do it right.  It is n’t about the money – it is about making sure that the best education is made available to anybody who needs it.

So now – the boys are “putting the band back together”.  We are going over the evidence again, adding what is new and throwing out the dogma.  This will be a labour of love for me.  As you know I am an US tragic and this is a great chance to spread the word.  So over the next few weeks I shall be scouring the literature to find all the newest and funkiest trauma tricks in Advanced Bedside Trauma Ultrasound.  How far can we extend the E-FAST?

A Special Project…  [secret squirrel]

Not being busy enough I have taken on a new job in 2016.  It is hopefully going to be huge!  When I started Broome Docs I wanted to be able to create a resource where doctors like me could go to find all the information they needed.  I wanted a place where we could learn new skills, find a quick answer and share ideas.  The blog and podcast have served the purpose and I have learned a heap in the process.  So now I want to take what I have learned and create something that will hopefully fulfil my original vision and become a future-proof.  I’ve joined a team of super-smart Docs and great educators with the goal of making Emergency Medicine Education in WA what it ought to be.

Ultrasound Leadership Academy

Two years ago I joined the ULA as a founding “Professor”.  We have been teaching all over the globe and the students have started teaching their students.  This is an immensely rewarding gig.  I have had the opportunity to met some amazing clinicians from all over the place – many working in places where resources are scarce.

World ULA

In 2016 I will continue to do my bit for this great project.  We Hangout with our students for an hour every few weeks and go over cases, share tips and learn from one another.

If you are a teacher and want to try out this technology – I highly recommend it.  We have been using it for a few years and it has become easier as the software has evolved.  I really think the Aussie rural GP folk should be embracing this sort of medium – geography is no longer a barrier to quality tacit learning.

My Day {often night} Job

Well – this is the one that pays the rent!  Working in beautiful Broome continues to throw up all sorts of clinical challenges and conundrums.  Broome has become a real hot bed of Med Education over the last 5 years with lots of super keen colleagues, students and trainees.

Next week we will welcome our latest batch of JMOs and students – and I am looking forward to it.  I have had the great fortune to work alongside some really excellent young Docs in the last few years [you know who you are!] and it is very satisfying to see them go on to do great things.  So I cannot wait to meet the next bunch and start learning together with them into the future.


So that is a bit of a peek behind the scenes.  Lots stuff happening.  A few big, long term projects which will mean maybe a little less of the stuff you see and hear here on the blog.  As always I really love to hear from you out there.  If you have a case or a clinical question that you would like to share – please do.  Just email and I will do my best to find an answer, share your thoughts or pass it onto the really smart folk I have met over the last 5 years.

Have a great 2016.  May all your tubes go into the right places!



UKCTOCS: Ovaries, P-values & Questions

Ovarian cancer is a horrible disease.  It is often asymptomatic until late in its course and then causes a lot of suffering.  This is a disease with an extraordinarily high morbidity and currently has a 5-year survival of only 40%.  So wouldn’t it be excellent if we could find this disease early in it’s course, intervene and cure it?

This has been the goal of several large population screening studies over the last few decades.  To show that screening and subsequent early detection will improve the outcomes for women with ovarian malignancy. Last week the LANCET published the latest mega cohort – Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial

This is the largest ever trial looking at ovarian cancer screening – with more than 200,000 participants randomised and exceptionally well followed and documented.  This trial was roughly twice the size of the Ovarian component of the American PLCO trial published in JAMA in June 2011  .  The American PLCO trial failed to find any benefit from screening for Ovarian Cancer and did find a significant burden as a result of over diagnosis, false-positivity and subsequent downstream complications.

So many people in the medical community have been awaiting the outcomes of the UKCTOCS trial – and on the 17th of December it landed.  So – what was the outcome?  Did they find a benefit?  Will we be changing our practice based on this new data?  Well this is where it gets interesting.  The UKCTOCS trial has been publicised widely as “positive” result – i.e. a significant benefit for screening.  However, when you read the paper things are really not so clear.  In fact – they are quite unclear… muddy.  So I am going to do a bit of a deep dive into the paper and try to make sense of it all.  But first lets look at the coverage in the mainstream and medical media.  You need to know what your patients are hearing and go beyond the sound bites in the medical media to get this one right.

In Australia the two biggest medical News rags reported the trial very differently:

So if you are the sort of doctor that reads the headlines and skims the abstracts then you are probably getting some mixed messages.  Unfortunately both of these articles didn’t delve into the statistics underlying the claims made in the discussion by the authors.

In the USA the mainstream media also reported this important trial with similar headlines.

CBS News was very positive, the headline was: “Blood test for ovarian cancer saves lives, study finds” They interviewed a few Medics and if you read the article the benefits are clarified and it is suggested that we need to wait 3 more years to check if it really works.  But the expert interviewed, Dr Agus, is quoted as saying:”If this [screening] were implemented in the United States we would save about 3,500 lives per year,”  Interesting …. that is the sort of statement that tends to have patients knocking down our doors to get this new ‘super test’.

The New York Times was more circumspect.  They interviewed Dr Menon – one of the lead authors.  Their headline was: “Early Detection of Ovarian Cancer May Become Possible”  They published a series of bites from a range of expert medical professionals which ranged from positive, through to skeptical and did include a number of the key statistical points.  The NYTimes also made note of the author’s potential conflict-of-interest.  This was probably the most rigorous coverage of the trial I have read.

So you need to know what the UKCTOCS trial did and did not find.  Your patients will be asking you for advice and may request the “test”.  So lets break it down and look at the study.  Lets do a super PICO analysis.

POPULATION: This was a huge trial! 202,638 women were randomised.  They were between 50 and 74 years of age at randomisation.  They were largely postmenopausal. The study was completed in the NHS Trusts from all over the UK and Northern Ireland.  More than 96% of the participants were “White” – so a very Anglo population.  As you might expect from such a large cohort – the baseline stats were all very evenly matched across the groups and a good representation of the sort of patients that we all see and treat.  Variables like age, menstrual history, HRT use, parity and co-morbid cancers were what you would expect.

More than 1.2 million women were invited to screening from the massive NHS databases – the idea here was to minimise the effect of the “healthy volunteer effect”[HVE]  which can skew results in screening trials – i.e. make it less likely to find as many cancers if all of your volunteers are clean living, non-smoking, health conscious folk.  The authors of the UKCTOCS also published an analysis of the “healthy volunteer effect” in 2011 in Trials.  However they concluded that their invitation strategy did not reduce the HVE – this kinda makes sense when you consider that only ~ 1 in 6 women accepted the invitation to participate.  I imagine they would represent the health conscious upper 1/6th  of the population!  The HVE meant that the women who participated in the trial died at a particularly low rate – overall only 37% of the predicted mortality.  So the external validity of these results are difficult to apply to the population as a whole.

Importantly it should be noted that women at increased risk [defined as > 10% lifetime risk] of ovarian cancer due to family history (

Eligibility was determined as follows: Participants were known carriers of one of the OC predisposing genes (BRCA1, BRCA2, MLH1, MSH2, MSH6, PMS1, PMS2) or first-degree relatives (mother, sister, daughter) of an affected member of a high-risk family. High-risk families were those fulfilling any of the following criteria: The family contained two or more individuals with ovarian cancer (OC) who were first-degree relatives The family contained one individual with OC and one individual with breast cancer diagnosed at age < 50 years who were first-degree relatives The family contained one individual with OC and two individuals with breast cancer diagnosed at age < 60 years who were connected by first-degree relationships The family contained an affected individual with a mutation of one of the known OC predisposing genes (BRCA1, BRCA2, MLH1, MSH2, MSH6, PMS1, PMS2) The family contained three individuals with colorectal cancer, at least one of whom was diagnosed at age < 50 years as well as one individual with OC, and all of these individuals were connected by first-degree relationships The first three criteria could be modified where paternal transmission occurred (ie, families in which affected relatives were related by second degree through an unaffected intervening male relative and in which the proband had an affected sister were eligible) In addition, when women did not fall within these inclusion criteria, but the recruiting center felt that they had a lifetime risk of OC of ≥ 10%, the study clinical geneticist (J.M.) reviewed the pedigree and documentation of diagnoses to determine eligibility.
) were excluded from the trial.  They were invited to join the UKFOCSS trial run by the same group.  See the end of this post for a discussion of that trial.

INTERVENTION:  the women were randomised 1:1:2 into 3 groups.  There were 2 separate intervention groups each consisting of more than 50,000 women.  Obviously the women and clinicians could not be blinded to the intervention, however the outcomes team were masked when analysing the clinical outcomes.

The original protocol was for 6 annual screens and 7 years of follow-up.

The compliance with the screening protocol was about 80% which is roughly the same as similar large population-based screening trials.

However, as noted above, the healthy-volunteer effect messed with the calculations.  The mortality rate of the trial participants was much lower than that expected in the general population.  The women in the trial died at 37% of the rate anticipated at the outset and by the end of the 7 years only at about half the mortality rate expected.  This is an issue.  Less deaths means that there was less potential to detect a real difference in the groups – the efficacy of the screening would be watered down by the relative good health of the participants. However the healthy volunteer effect also means that there are likley fewer deaths from other causes – so may bias the data to make screening look better than it is… but we don’t know for sure. See discussion of “all-cause mortality below”.

The research team decided to extend the screening period by 3 years in order to improve the ability to detect a difference.  In plain speak – they increased the ‘dosage of screening’ to find try and detect a benefit.  Subsequently follow-up was also extended… median follow up was about 11 years at the final curtain.  The extension resulted in a recalculation of power to detect a 30% difference from 90 to 80% power.

So here is how the screening tests went:

  1. Ultrasound screening: women underwent annual trans-vaginal ultrasound and were followed up as follows:
    • Normals – ongoing annual screening scans
    • Unsatisfactory – had a repeat scan done in 3 months
    • Abnormal scan – these women had a repeat scan with a senior sonographer within 6 weeks.
  2. Multimodal screening (MMS)
    • This screening strategy was a bit more complicated.  It is based upon annual CA-125 blood levels.  Women were tested and their results fed into an algorithm called ROCA [Risk of Ovarian Cancer Algorithm] to detect rises in CA-125 over baseline, rather than using a standardised lab cut-off.
    • The ROCA algorithm triaged the women into three groups:
      • Normal: continued annual screening
      • Intermediate: repeat CA-125 in 3 months
      • Elevated: these got a repeat CA-125 and a TV ultrasound within 6 weeks
    • Important note: Prof. Jacobs, the lead author declares in the COI statement that he holds the patent for the ROCA algorithm and has financial interest in the company Abcodia which sells this test.

Women with persistently abnormal results – either on US or the ROCA/US groups were subsequently investigated clinically by a trial investigator.  They received whatever investigations or surgeries that the specialists thought were required.

There were a few papers written by the UKCTOCS team in 2011 analysing the relative sensitivity and specificity of each of the screening modalities. Both were around the 80 – 85% mark.  Of note screening detected a little over half (59%) of the tumours counted in the total of ovarian cancer deaths.  So at best screening will find a bit over half of the nasty tumours.

CONTROL:   About 100,000 received No Screening (although there was some contamination of the control group – as would be expected in such a large study.) 4.3% of women underwent some sort of screening in the control group based upon a questionnaire at the end of the trial.

OUTCOMES: The primary outcome used in this trial is ovarian cancer death by Dec 31, 2014.  Below is the key table of results form the paper:

Summary mortality

Note – this is a disease-specific mortality outcome.  There was no mention of “all cause mortality”.  The trial was powered to detect a 30% mortality benefit for screening.  There is no data provided in the paper about “all-cause mortality”.  This is a bit odd as the best measure of the effect of a screening intervention would be “all-cause mortality”.  The use of disease-specific mortality is useful to tell us if the screening actually does pick up cancers earlier and prevent death from ovarian malignancy, however….  we, and our patients, want to know if it will make them live longer.  Only all-cause data can tell us this.  If screening means that we diagnose ovarian cancer early and then we increase other mortality eg. more PEs or surgical deaths then we are not doing the right thing by our patients.

I did email the authors and ask if there were any numbers on “all-cause” mortality.  The response did not throw any light on this stat.  I do find it a little unusual that in such a large, well-conducted trial with great follow-up that this data was not published as part of the trial.  Even if it were included as a secondary outcome – we could at least look and get a feel of the overall benefits.  So I remain a bit confused as to why it didn’t get included.

Ovarian cancer was defined as: “malignant neoplasms of the ovary, which include primary non-epithelial ovarian cancer, borderline epithelial ovarian cancer, and invasive epithelial ovarian cancer; malignant neoplasms of the fallopian tube; and undesignated malignancies of the ovaries, fallopian tube, or peritoneum.”

Specifically primary peritoneal was not a primary outcome – although the WHO reclassification of cancers in 2014 threw a bit of a spanner in the works.  The analysis therefore includes a “secondary analysis” which includes both primary ovarian cancer AND primary peritoneal cancer in the mortality numbers.  Hmmm… not sure about his one!  Beware the analysis of secondary outcomes

The analysis also broke the mortality reduction numbers into two time periods – 0 – 7 years AND 7 – 14 years.  This is an interesting way to crunch some numbers.  As with any long term mortality study – it is a basic fact that more people die the longer that you follow them.  Hence there is more likely to be a benefit shown later in follow up.  So if you are trying to break through he magical p < 0.05 line – then this is one way to do it.

Now if you scan the table above you will notice a few things:

  1. There are two different statistical techniques used to analyse the data – the Cox model and the Royston-Parmar model.  These are both accepted ways of looking at data such as the survival data in this trial.  However if you go back and look at the UKCTOCS trial protocol (available here at IWH website ) you will read the planned analysis was “a Cox regression model will be used to model the difference in mortality rate between the control arm and each individual screen arm.”  So the Royston-Parmar model was not originally planned.  Is this a problem? Well suppose we used 20 different models to analyse the mortality curves and then only published the one or two that showed a benefit.  This is why we have a trials register – to ensure transparency of trial design and analysis.  Note: Prof. Parmar was the head statistician on the UKCTOCS trial – so understandable that his method was used as an analysis tool.
  2. None of the Cox models reached statistical significance – they all included “0” in the confidence interval.  However the R-P model did just squeak under the P-value of 0.05 for a few of the stats – namely those where “prevalent cases were excluded”  which brings me to  point #3.
  3. “Prevalent cases” were excluded from the analysis.  Makes sense – we should not include women who already have ovarian cancer at the outset.  But… hang on a minute.  How did they know that these women had a cancer before they started screening?  Well it is hard to answer that question.  It appears that they looked at the CA125 trend in women who were diagnosed with ovarian cancer and extrapolated backwards in time to decide which women likely had a tumour at day 1.  Hmmm… so how did the women in the “no screening” group get the same treatment if they never had a CA125?  They did a post hoc assay on stored serum samples from enrolment samples and decided who probably already had a ‘prevalent cancer’ based on the CA125 level.  I do not understand how we could generalise this to an external population of real world women.  We can never know who already has a tumour in day-to-day GP practice ( if the women are asymptomatic) – so excluding them from the analysis seems to reduce the external validity of this trial.
  4. The analysis was extended to include both Ovarian and “primary peritoneal cancer” as a composite secondary.  This also makes sense – primary peritoneal cancer is likely ovarian in origin as per the WHO reclassification.  However if you look at the raw numbers you will see that the inclusion of this secondary outcome does favour the MMS strategy – there were 16 peritoneal cancer deaths in the MMS group and 15 in the control group.  Recall that the control group was twice the size of the MMS group.  So although it is a reasonable thing to analyse we need to beware of secondary outcomes and composite outcomes as they will be prone to bias.
  5. Of the screening groups 1634 women [50 per 10,000 screens] had unnecessary surgery i.e. surgery that yielded benign results.  The rate of “false positive” surgery was described by the ratio of benign : malignant pathology.  The ratios by group were : No-screening = 1 : 1.2,  MMS 2.7  and USS 1: 6.4 .   The surgical complication rate is quoted as 3.5%.  Unfortunately the actual harms of the surgeries were not documented as far as I can tell from the paper.  They are discussed in the 2-hour video produced at the trial launch – but bizarrely not in the actual paper. So it is hard to say what the actual true “harms of screening” are in this study.  Below is the table you can find in the supplementary material which describes the types and numbers of harm events in the screening groups.  For the record – in the PLCO trial the surgical complication rate in screened women was ~15% – so 5 times higher than the UK group…  must be better surgeons in the NHS?Screen Shot 2015-12-28 at 9.53.46 PM


There was a retrospective review of the American PLCO population data where they went back and applied a “best guess” version of the ROCA algorithm to the American cohort. Titled: Potential effect of the risk of ovarian cancer algorithm (ROCA) on the mortality outcome of the Prostate, Lung, Colorectal and Ovarian (PLCO) trial from Int. Journ Cancer, 2012.  In this exercise the authors wondered what if if they had used the ROCA algorithm instead of the absolute CA125 cut-off value as a screening tool?  Of course this has to be taken with a grain of salt – but they concluded that ROCA would not have shown any additional survival benefit in the PLCO cohort.  One of the authors, Dr Skates, is also a co-inventor of the ROCA algorithm and co-author of the UKCTOCS trial.

There was another subgroup trial within the UKCTOCS cohort which examined the psychological impact of screening on the participants.  Titled: Psychological morbidity associated with ovarian cancer screening: results from more than 23 000 women in the randomised trial of ovarian cancer screening (UKCTOCS) published in BJOG in Feb 2015.  This was a prospective RCT which measured anxiety levels among women undergoing screening and subsequent investigation and surgery. The basic findings from the psychological surveys?

  • Being screened did not seem to increase anxiety
  • Having to have subsequent testing after an initial positive screening test did increase anxiety
  • Undergoing surgery increased anxirty
  • Being diagnosed with ovarian cancer had a large effect on anxiety – as one might expect.


The same research group also offered screening to “high risk” patients in a separate trial mentioned above – UK FOCSS.  This was a prospective observational study (no control group) looking at the performance of annual screening using CA125 and TV ultrasound in 3500 high risk women.  The screening was found to be 80% sensitive.  And in this group there was not a significant “stage shift” in cancers detected.  That is – screening did not move women from an advanced stage of disease at diagnosis to earlier, more treatable disease.  There were a few reasons discussed for this finding and the trial is now in Phase II – in which women are screened at 4-monthly intervals and faster follow-up surgery etc are planned. So in summary – even in a high risk cohort we have not yet seen a benefit from annual screening in terms of finding earlier disease.  That is the core goal of any screening program – to find earlier and treatable disease.


I am “just a GP”.  I am not a guru in biostats so I may be completely wrong here.  However, I am just a GP who wants to know what to tell my patients when it comes to screening for a nasty disease.  I would love to be able to do something to prevent my patients from getting diagnosed with late-stage ovarian cancer.  Here are my summative thoughts:

  • The UKCTOCS study was large and well conducted.  The results, in my reading, do not show a significant benefit to screening.
  • There are a number of statistical and methodological quirks that do raise questions about the reliability of the results and their external validity
  • The conclusions of the authors are optimistic – yet at the basic scientific level – we cannot reject the null hypothesis based on these numbers.
  • In time we may get more follow-up data which may change the situation.  However, as of December 2015 I do not think we should be changing our practice.
  • Screening for ovarian cancer remains unproven and the harms remain largely unknown.
  • I would really likely see the all-cause mortality data presented in a clear manner so that we can all look at it and make our own conclusions.

Based upon my reading of this paper and the surrounding data I do not think I will be recommending screening with any tool for ovarian cancer to my patients.

I am somewhat concerned that this paper and the media hype around it may represent the “edge of the wedge” – a foot in the door for screening which remains unproven.  We have all seen and struggled through the perils of prostate cancer and mammography over-diagnosis.  At best guess the “number need to screen” is somewhere between 2000 and infinity.  This is a very weak effect if any at all.  We should be investing our time, money and patient’s goodwill in other health pursuits for now.

Love to hear your thoughts