AusMAT Bravo on the way to the Philippines

Team Bravo heads to Tacloban to continue the “shining light” that is the Australasian AusMAT medical response to Typhoon Haiyan. Be safe guys.

AusMAT in Tacloban after Typhoon Haiyan

I just wanted to share here a link to an ABC write up of the AusMAT deployment in Tacloban after Typhoon Haiyan. Ian Norton and Mark Little are out there leading a team of dedicated folk around the clock, and will soon be relieved by a second team going out this week, led by Nick Coatsworth and our own Jo Kippax. Be safe guys.

Busting the clotbusters (from SMACC 2013)

As revenge for an incident best left unmentioned, Chris Nickson of and handed me the poisoned chalice of speaking on tPA for stroke at SMACC 2013. This is the result. (Un)fortunately there is no actual video footage as I wasn’t important enough, so my Finnish heavy metal air cello will be left to your imagination. The first embed is the audio plus slides, and there is an audio only version below that (which doesn’t work so well – the visuals are kind of key at times)
The slides/audio combo:

Busting the clotbusters from Domhnall Brannigan on Vimeo.

The audio only:


Dundrum Quay (posted in tribute to Seamus Heaney)

Barnacle encrusted stumps remain.
Thrusting, vertebral fossils
From tidal glar pools and rising silt.

The bar is no longer dredged:
Time gently smudges over noisy, dark,
Dangerous memories:
Hard men stooping –
Their iron shovels grate on coal,
Organic metronomes in coal boat bellies.

I remember dimly the last coal boat
That hove to at the quay, then slipped away,
Leaving coal dust to settle, like age.

I’d leap and dive from great stone steps
Measuring days in the high tide times.
I fished here for pollock with dead-man’s-fingers
Torn cruelly from tortured crabs.

But now, luxury seafront apartments crowd
Like schoolyard bullies on the harbour walls
And the silt rises as the stories die.


Health care – do we (and HOW do we) really CARE?

this post first appeared on my original blog, the underneaths of things, and I was prompted to repost it by Andy Neill of linking back to it:

This is a re-post of a rant I let slip on a colleague’s FB page – he had just published an article in the local rag (The Mercury) with some great points about future directions in health care provision. His article is republished in the Tasmanian Times HERE. I agree with much of what he writes, and was moved to stick my oar in just a little (nowt new there, I hear you cry). My tuppence was this:

“Let’s put the onus in health care on CARE as the goal rather than on DIAGNOSIS as an intellectual pursuit of intrinsic value for the patient (i.e. we need to rank caring for our patients above a “House-like” detective approach to diagnosis – “see, you have a diagnosis now – you are still going to die, but I, your doctor, feel much happier and you should too!” – somehow we have even convinced the patients that having a label is intrinsically better for them).
Then, if we prioritise CARE over DIAGNOSIS, we might be able to limit overuse of expensive tests that don’t change the outcome for the patient, and put more money and energy into public health, and education about acceptance of illness and death as a normal part of life!”

Of course, if the public (that faceless entity) is happy to keep paying taxes to fund an increasingly inefficient, wasteful and expensive health care system, then that’s fine, but we can’t have it both ways! You don’t hear a lot of people say that they are happy for their taxes to be poured into the drain…

The flipside to this is that it is us as a profession that has created and nurtured unrealistic expectations in our patients (not the lawyers and the media – they just feed on what we give ’em) and so it really must be our responsibility to remould these expectations. We need to tell our patients the truth. Sometimes, we (as in “we in modern medicine”) just don’t know what is wrong with you. Sometimes, we know what it is, but we don’t know how to fix it. It should be OK to say that. In fact, it should engender trust in the relationship. Frustration, sure, but in the doctor-patient relationship, trust is much more important than keeping a veneer of omniscience. As a good friend, who is very much a thinking physician, once said to a student – “you can’t just make shit up!”

If you don’t know…or more accurately if WE don’t know – SAY SO – it is liberating, I assure you!

Imagining the future

This is the footage from one of the sessions I chaired at last November’s ground-breaking ACEM ASM in Hobart. The theme of this session was “Imagining the Future” featuring Kendall Ho, Mike Cadogan and Stephen Atherton. It’s long, but there is some good stuff in there. Excuse the mumbling chairman…and the lack of audio in some parts of the Q+A after the talks.

tPA – black and white or shades of grey?

This is a micro-post just to illustrate yet another problem with the Boehringer Ingelheim/Neurology juggernaut pushing the Emergency Medicine community towards lysing anyone with a tingle.

Ryan Radecki just posted this little vignette on the real incidence of stroke mimics (AKA “neuroimaging negative” stroke) with the associated reference on emlitofnote:



This is the first in what will hopefully be a series of posts by new recruit Dr Kate Field, an Emergency Physician based at Calvary Hospital in Hobart. In this episode, Kate takes a look at the dogma and assumptions underlying the most commonly (un)prescribed drug delivered in our Emergency Departments.

Subsequent posts will more closely examine the evidence for O2 use in cardiac chest pain, COPD/asthma, pneumonia, sepsis and traumatic brain injury (TBI).

So let’s inhale deeply, fill our FRC with fresh air, and see where Kate takes us:

photo (26)

Oxygen 1: friend or foe?


I became interested in this question a couple of years ago when I was informed by an RN in a regional Australian hospital that they “aren’t allowed” to give high-flow O2 to patients (with normal pulse-oximetry readings) presenting with cardiac-sounding chest pain “because free radicals make myocardial damage worse”.

At the time, as a very fresh consultant/attending Emergency Physician, I felt like I may have missed something important and felt somewhat chastised by my nursing colleagues. I decided to investigate the evidence for O2 therapy in a wide range of conditions.

Traditionally, we were taught that administration of high-flow O2 is standard practice (think back to EMST, APLS and ATLS teaching) for all patients who are critically unwell, and definitely for all cardiac patients. The exception that proved the rule was the chronic CO2-retainer with COPD, but even then, if they were severely hypoxic, they received life-saving O2 (high-flow if required), given the oft-quoted axiom “hypoxia kills quickly, hypercapnia kills slowly”.

But could we have got it wrong? Have we been inadvertently harming our patients?

Some of the questions arising in my quest include:

  • What is ideal PaO2? What is the definition of hyperoxia?
  • What does hyperoxia and free radical generation really do, other than cause wrinkles and help sell expensive face-creams to aging women and Sydney men?
  • Does ideal PaO2 vary in individuals?
  • Is there individual variation depending on biological or pathological processes that are occurring; what is that patient’s ideal PaO2 considering the disease state they are in now?

What I discovered is that there is very limited evidence in the literature.

I was able to establish that “normal” PaO2 on room air (FiO2 = 0.21) at sea level is considered to be 75-100 mmHg. How this translates into individual variation throughout the course of a lifetime varies on patient factors and also disease factors (e.g. smoking, auto-immune disorders, occupational exposures, etc.). Expert consensus suggests that as long as your PaO2 is > 50 mmHg, you’ll be OK. Looking at the Hb-O2 dissociation curve, this roughly correlates with a SpO2 of 85%.

Click here for a refresher on respiratory and Ophysiology.

(If textbooks are still your thing, check out West’s Respiratory Physiology).

HbO2 curve from #physphoto118

Individuals will have times during disease burden where they actually have increased O2 consumption. Examples include:

  • Fever: with a 1oC temperature rise, there is a 7% increase in O2 consumption
  • Seizing patients (even if given muscle relaxants): still exhibit a 300-400% increase in O2 consumption in their brain.
  • Septic patients: demonstrate 200% increase in O2 consumption.
  • In exertion/exercise (think seizure, rigors, restlessness, increased work of breathing) your O2 consumption is also going to increase.

How does this information translate to our practice?

The effects of hyperoxia are more variable than just simple free radical production: Hyperoxia can directly affect blood vessels, causing vasoconstriction. At the level of the pulmonary vasculature, this can worsen V/Q mismatch. Vasoconstriction of coronary arteries and cerebral arteries probably isn’t really a good thing either!

How do free radicals actually cause harm? Free radicals are generally mopped up by nitric oxide (NO – the chemical that vasodilates vessels in vivo). They have direct cellular effects, including harming DNA, and can even cause apoptosis of cells.

What is the EVIDENCE for the role of free radicals?

I found this article, which I have to include:

first paper

The authors comment that:

“The use of oxygen in “severe angina pectoris” was first described in 1900 by Steele. Clinical improvement after oxygen inhalation in four patients with acute myocardial infarction was reported by Levy and Barach in 1930. Since then the use of oxygen in myocardial infarction has been advised in most standard medical texts.”

(As an aside, I am amazed that “clinical improvement” in only 4 patients in 1930 became standard of care. What else are we doing that has such profound evidence?)

The 1976 BMJ study was a double-blinded RCT which randomized 200 consecutive patients thought to have had MI to treatment with O2 or air, administered via medium concentration mask for the first 24 hours of hospital care. 43 patients were excluded post-hoc when diagnosis of MI was revoked. None received current standard MI treatment (aspirin, thrombolysis, PCI), so the applicability to current practice is somewhat debatable.

There was a mortality rate of 11% in the O2 group vs. 4% in the air group, but this did not achieve statistical significance.

They conclude that the results are suggestive that O2 administration has a “deleterious effect”, and that administration of O2 in patients with an uncomplicated MI does not have any benefit.

[This went unnoticed until unearthed in a systematic review (by Wijesinghe et al. in HEART 2009) of the…wait for it…two, yes, TWO relevant papers in the literature on the subject!

ILCOR and ARC ran with this in 2010-11, and an RN in a regional hospital quoted it back at Kate shortly after – Domhnall/Ed.]

Cementing our move into the 21st century, 2012 brought this paper:


The study:

  • This was a randomised, controlled trial with n = 136.
  • All patients presented with an uncomplicated STEMI (i.e., no cardiogenic shock or “marked hypoxia”).
  • The 2 groups were randomised to receive either “standard of care” (6L/min via medium concentration mask) or titrated O2 aiming for SpO2 93-96%.
  • The primary end-points were 30-day mortality, and infarct size (determined by the Troponin T level at 72 hours)
  • They also utilized MRI at 4-6 weeks for a subset of patients to assess infarct size as a secondary end-point
  • The result was that there was no significant difference between high-concentration O2 vs. titrated O2 in regard to Troponin T concentration, infarct mass or percent infarct mass.

Problems with the study:

  • Small study with wide confidence intervals – the study should probably be repeated with a much larger sample size to truly determine if there is harm/benefit associated with supplemental O2
  • Unblinded study – but, primary end-points were objective measures, so shouldn’t alter the outcomes
  • Pre-hospital O2 therapy (received PRIOR to enrollment in the study) – patients averaged 62 min of pre-hospital O2. Does this have an effect? It certainly muddies the waters for me…
  • There was a significant difference in the two groups with respect to the territories infarcted: more in the high-flow group had an inferior or posterior MI, compared with those in the titrated group with an anterior MI. Those with an anterior MI tended to have higher peak troponins; however this did not lead to a statistically significant difference in the groups

Finally Nikolaou et al. in an opinion-piece in the Hellenic Journal of Cardiology, published in 2012 (53: 329-330) argue that:

“inhalation of 100% O2 for 10-15 minutes is associated with a decreased in coronary blood flow by 20-30% through constriction of the micro vascular resistance vessels”

They hypothesise that this may be due to NO being depleted by mopping up the free radicals generated through hyperoxia. They cite an additional concern that hyperoxia may exacerbate reperfusion injury to the heart (due to increased free radicals).

They conclude that evidence is lacking, but despite this, go on to recommend that

“routine administration of high-flow O2 for ALL acutely ill patients should clearly be abandoned and be replaced with judicious O2 administration guided by pulse oximetry”

I’m rather (un)impressed that they have managed to draw this very concrete conclusion for acutely ill patients (with any aetiology) in a cardiology journal, based on a carefully selected 12 papers, of which 11 are specific to cardiology (the exception was the BTS guidelines for emergency O2 use in adult patients). It really is a bit of a leap, however, this is where I stand:

My conclusions in regards to O2 for ACS:

  • We still don’t know if we cause harm, or benefit, by giving our patients high-flow oxygen when they have myocardial ischaemia.
  • We just don’t have evidence to say that what we have considered as standard of care for years (i.e. 6L/min O2 via Hudson Mask) is harming or benefiting patients in this and other groups of acutely ill patients.

Will my practice change?

  • I think I will probably remove more Hudson Masks now and replace with titrated nasal prongs, if required, aiming for SO2 of 95% (why that number, I can’t say, but it’s what I feel comfortable with and it is within “physiological normalcy”).
  • More importantly, it makes it a hell of a lot easier to take a good history, which will probably benefit my patient more.




@TheTopEnd interviews underneathEM

Minh le Cong (@rfdsdoc) from down on the PHARM has hosted some of Doug Lynch’s (@TheTopEnd) “jellybean” interviews from the SMACC 2013 conference in Sydney last week. A selection of his chats (including one with Doug, Minh and I where we discuss my stroke lysis talk, Ireland, Tasmania, and the state of the nation) can be accessed here:

PHARM Podcast 64 : MORE Jelly Beans from SMACC 2013 with Dr Doug Lynch.


FOAM & SMACC craic – from outside the citadel


I’ve been thinking about FOAM since SMACC2013 (Social Media and Critical Care)…thinking a lot and talking to some friends.

I’ve cleared my desk literally and figuratively for a while and intend to read a lot and spend sometime away from computers and in the fresh air. But for good or ill I’m going to share some of my ruminations about FOAM post-SMACC and where it stands:

I thought SMACC was an amazing conference, and I had a fantastic time. I was inspired and challenged by many, especially some icons of the Critical Care world – Cliff Reid, Scott Weingart and Joe Lex. Meeting them, and others, as if I had known them for years, was a surreal experience. I also got a real buzz from speaking among such eminent company and not self-destructing, despite my extreme anxiety about it (or perhaps because of my anxiety – since as Myburg and Weingart say, adrenaline is “God’s own nectar”).

But among all of this enthusiasm, euphoria and exaltation, I have become aware that not everyone felt like I did about SMACC2013. Some people I have the utmost respect for, including several colleagues who I consider to be mentors in my professional life, had what they describe as a “mixed” experience. Rather than trumpet my own overwhelmingly positive experience, I thought it would a be useful exercise to explore the experience of others. So this will be an opinion piece discussing the discomfort of some with how the “Brave New World” of FOAM and #FOAMed is playing out. I think it is important to air and address these views in order to ensure that the “product” we deliver as FOAM is as good as it can be.

FOAM as espoused by SMACC is unfolding with some of the features of a new religion:


  • It has a “big idea” at the core.
  • It sets out to reject dogma and challenge the status quo.
  • It is somewhat anti-establishment.
  • It has evangelists. It has an inner circle of disciples, it has zealots and it has converts.
  • Thus, it faces the same problems as a religion, and could fall into similar traps, and could eventually leave itself open to some of the same criticisms as religions are.

There are several traps FOAM could fall into, I believe:


  • It could lose itself in enthusiasm, evangelism and quasi-religious fervour.
  • It risks the criticism that there is a “cult of celebrity” developing (I don’t think this is true, but it is how some see things from the outside).
  • It preaches openness and yet some see it as a clique. It can appear somewhat smug to the “uninitiated”
  • It risks portraying itself as the “one true path.”
  • SMACC spent a lot of time discussing ideas about how we can ensure that FOAM self-polices content and quality, but little time addressing the fact that there is risk that it develops into a “club” which some may not feel they can join.
  • Although a version of “peer review” is important, I think this perception of a clique is a bigger threat to FOAM.

The big ideas of SMACC2013 apart from furthering FOAM as an educational movement were: challenging dogma and destroying silos – particularly those separating pre-hospital medicine, ED and ICU. But we MUST be careful that we do not replace these silos with another silo, the FOAM silo. We must not just challenge the dogma that exists and then fall into the trap of creating a replacement dogma (The central message of a certain prophet/son of god/historical figure was love, equality, rejection of dogma and openness – but his followers somehow contrived to develop a new boys club and a new dogma as exclusive and prescriptive as what preceded it).

FOAM, and conferences like SMACC, risk alienating further the slightly more open and curious skeptics precisely BECAUSE they don’t feel part of the evolving club despite taking the courageous step of attending to dip their toes in the water. For those of us who, as Scott Weingart says, “jump in and drink from the stream” it seems self evident that you get out what you put in, but not everyone feels able to commit to that degree, and we risk losing the swinging voter unless we accept and address the perception that FOAM can appear like an exclusive inner circle to the outsider. This may seem crazy to us and is light-years from the intentions and principles of FOAM, but it is definitely how some perceive us. We think we are making it easy because it worked for us, but we need to be rigorous about how open the FOAM movement is.  So what can we do?


FOAM must remain truly open and inclusive.

FOAM must listen to and embrace the uncertain and dissenting voices.

Pretty simple, and yet I suspect it will be very difficult.


rants, rambles and random reason: exploring Emergency Medicine