whats happening in the EM world

the educators' blog: 

an online journal of whats impotant in emergency medicine, specifically as it relates to our local practice in the Hunter New England Area. please post comments via the 'post new entry' and upload any files into the appropriate folder under 'files'. 

 **please note this blog is available to the general public and anyone using it, in any fashion, is deemed in agreeance with our "terms of use" as described under our disclaimer 



Journal Club: Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Morrison et al

The study: This was a retrospective, observational, cohort study enrolling 896 trauma patients who had received at least 1 unit of packed red blood cells after admission to a single surgical hospital at Camp Bastion in Southern Afghanistan following a combat related injury. They compared the group of patients who had received tranexamic acid to those who had not received it.


Primary outcomes:

-Mortality at 24hrs, 48 hrs, & 30 days


Secondary outcomes:

-Transfusion requirements

-Coagulation parameters (prothrombin time & activated partial thromboplastin time): measured at 2 points: (1) admission to the ED of the surgical hospital & (2) admission to the ICU following OT

-Incidence of thrombotic events such as DVT or PE



-There was no statistically significant survival benefit using TXA within 24 hrs in either the overall group or the massive transfusion group.

-There was an overall mortality reduction in the TXA group within 48 hrs (11.3% vs 18.9% p value 0.004) & In-hospital mortality (17.4% vs 23.9% p value 0.03).

-There was a significant mortality reduction in the TXA arm of the massive transfusion group within 48hrs (10.4% vs 23.5% p value 0.003) & in-hospital mortality (14.4% vs 28.1% p value 0.004)

-In the overall group there was a statistically significant increase in the amount of all blood products (PRBC, FFP, Platelets & cryoprecipitate) used in the TXA group. This may reflect the increased severity in this group.

 -In both the overall & massive transfusion cohorts there was a statistically significant reduction in hypocoagulation in the TXA groups when comparing the patients bloods taken in emergency to their bloods taken in ICU following OT.

-In the TXA group there was a statistically significant increase in the number of pulmonary embolisms (2.7% vs 0.3% p value .001) & deep vein thrombosis (2.4% vs 0.2% p value .001). The number of venous thrombotic events in this study is too small to assess any independent risk of TXA. Due to the reduction in hypocoagulation it is plausible that the higher rates of thrombotic events relate to the TXA.



-This study suggests a survival benefit to giving tranexamic acid to bleeding trauma patients. This article suggests that this may be linked to clot stabilisation & reduction in inflammation.

-We should be considering tranexamic acid in bleeding trauma patients, particularly if they are haemodynamically unstable.

-TXA is included in our massive transfusion protocol.


Link to the article


Link to the full appraisal


Link to our massive transfusion protocol


Journal Club: Effects of tranexamic acid on death, vascular occlusive events, & blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial.

The study:  20 211 trauma patients with or at risk of significant bleeding over 40 countries & 274 hospitals were randomised to receive tranexamic acid or placebo.


Primary outcome:

-All-cause mortality within 4 weeks of injury


Secondary outcomes:

-Vascular occlusive events (MI, CVA, PE, DVT)

-Surgical intervention (neurosurgery, thoracic, abdominal, pelvic)

-Receipt of blood transfusion, units of blood transfused

-Degree of dependency

-FVIIa use

-GI bleeding



-All cause mortality at 4 weeks was significantly lower in the TXA group compared to placebo: 14.5% (1463) vs 16% (1613) (Relative risk 0.91 confidence interval (0.85-0.97) p value 0.0035

-The risk of death due to bleeding was significantly reduced 4.9% (489) vs 5.7% (574) RR 0.85, 95% CI (0.76-0.96) p value 0.0077

-Trend towards more vascular occlusive events in the placebo group

-No difference in transfusion & need for surgery

-Trend towards early treatment being more effective

-No statistical difference in FVIIa use or GI bleeding (secondary to small numbers)

-Degree of dependency: statistically significant improvement in the number of patients with no symptoms within the tranexamic acid group (14.7% vs 13.3%) however, in the other degrees of dependency there was no statistically significant difference.



-This study suggests that the early administration (within 3 hrs) of tranexamic acid to trauma patients with, or at risk of, significant bleeding reduces the risk of death from haemorrhage with no apparent increase in vascular occlusive events.


Link to article


Link to full appraisal


Journal club: Canadian C-spine and NEXUS rules


Neck pain post blunt trauma is a very common ED problem.

This review looks very briefly at the two main clinical decision rules used in these patients: NEXUS and CCR.

The link to the NEXUS and CCR article is here.

The link to the NEXUS and CCR analysis, and the CASP guidelines used are here.

One interesting feature that comes up going through the literature is that these decision rules were made with XR as the gold standard of imaging, something which has changed in the last few decades due to publications of papers showing XR having a sensitivity of roughly 50%[1].

However, both of these decision rules had very good follow up (telephone questionnaires in CCR and review of local neurosurgical records and quality assurance logs in NEXUS) without missed injuries being identified.  Not sure what to do with that!

Personally, when possible I prefer to use the CCR rule due to the higher specificity, addition of ROM and a study[2] which compared CCR to CT which showed no missed injuries (Population 3,200 with 192 fractures).

This article was interesting in that it’s results suggested that the CCR rule had a specificity of only .6% for C-spine fractures…which again I’m not sure how to interpret.

 It’s reassuring to know that none were missed however.       

Would be very keen to hear how other people approach this problem.



[1]Mathen R, Prospective evaluation of multi-slice computed tomography versus plain radiographic cervical spine clearance in trauma patients, Journal of trauma, 2007, 62(6) 1427

[2]Duane T, Canadian Cervical Spine rule compared with computed tomography: a prospective analysis, Journal of Trauma, 2011, 71(2), 352-355.


3AM Rundown: Sympathetic acute crashing pulmonary oedema

Those that listen to Scott Weingart on EmCrit will recognise that this is basically taken from his podcast on SCAPE.

I’ve used the management plan on a number of patients’ now and find it really effective.

Saved me a couple of intubations.

If you want some more information or a more entertaining presentation I would recommend checking out podcast 1.

Should emphasise that this algorithm is geared towards the typical 6am patient presenting with marked sympathetic overload (diaphoretic/hypertensive) and signs of acute pulmonary oedema as compared to the patient with a bit of fluid in their lungs secondary to CCF

Run down:

  1. Pathophysiology: Afterload mediated heart failure.

- Aim of treatment is to decrease SBP rapidly and remove the oedema from the lungs with PPV

    2.   Treatment:

- PEEP: Start at 6-8 and titrate up to 10-12 as tolerated

- GTN Infusion: Loading dose of 400mcg/min for 1-2 minutes (or until lose radial pulse) and then decrease to 60mcg/min.

- Dosing using our infusion concentrations: 50mg in 500mls = 100mcg/mL

- Would start the infusion at 240mls/hr and decrease to 60mls/hr after any of the endpoints below:

  •          SBP normalising
  •          Infusion lasting 2 minutes
  •          Losing radial pulse (it comes back quickly!)

Titrate to blood pressure: Goal roughly SBP of 120mmHg

- Can use low dose captopril once patients stabilised to facilitate weaning of GTN drip (3.125mg-6.25mg)

- Don’t waste your time with frusemide: GTN more effective and patients with SCAPE can often be volume deplete.

If you have any thoughts/criticisms about this protocol feel free to post in the comments.



3AM Rundown: Automonic dysreflexia

The idea for these posts are to have some brief rundowns/management plans for critical pathologies that may come in overnight when you don’t have the time/head space to review the correct management.

If you had any additional thoughts/tips for the topics covered then please feel free to add those in the comments…any suggestions would help make this resource much better.

The first post is on autonomic dysreflexia.

I’ve only seen two patients with this, and the algorithm listed was incredibly helpful in working through the issues.

Algorithm listed here.

The Rundown:

1. Pathophysiology: Loss of coordinated autonomic responses to stimuli due to spinal cord damage above T6

2. Important tip: Normal blood pressures concerning in spinal patient.

- If SBP > 20mmHG above resting BP = Autonomic dysreflexia till proven otherwise

3. Symptoms: Headache/flushing are concerning

4. Causes: Retention and constipation big two.

- If not these then a head to toe exam for other painful stimuli required.

5. Why concern?: Hypertensive crisis. Seizures/Cardiac arrests/ICH

6. Treatment: As per algorithm.

7. Who to call for help: Rehab physician unless at large centre (Spinal Consultant)


Could this be Necrotising Fasciitis: The LRINEC study

I recently undertook a literature search surrounding this, after I was asked the question on a shift and found out that I really had no idea how to distinguish between necrotising fasciitis (NF) and severe cellulitis.

Unfortunately, it appears that this is a common issue, with the largest trial showing that only 15% of patients with NF were diagnosed on admission.

Which is a problem, seeing as the main predictor of mortality is time to surgical debridement.

Thankfully there are some tools to help us with this, in particular a clinical decision rule (LRINEC), bedside US, and the “finger test”.

The link to the LRINEC study is here

This was analysed using the CASP questions on clinical prediction rules: Analysis.

- For Questions please reference CASP UK website

The link to the finger test description is here.

- Page 1027 of this article or 1539 of the LRINEC study.

The link to the US study is here.

- Videos of normal and positive US are listed as well.

Bottom line:

1. Pathophysiology: Rapidly progressive infection involving the fascia and subcutaneous tissue with thrombosis of the cutaneous microcirculation.

- Moves from horizontal to vertical plane of spread.

2. Mortality rate = 34%. 

- Early operative debridement key to decreasing mortality.

- Appearance early difficult to distinguish from cellulitis or abscess

3. Clinical triad: Exquisite pain (98%)/swelling (92%) and fevers (80%)

4. Appearance: Initial = Redness with ill-defined borders.

 - Horizontal plane: Rapidly progressing with severe pain and tenderness beyond apparent area of involvement

- Vertical plane: Bullae →Gangrene (Necrosis/ulceration/crepitus and SC emphysema)

5. Investigations:

- Bedside US = STAFF examination:  Subcutaneous thickening, air, fascial fluid = 93% Specific

- LRNIEC scoring system: Score ≥ 6 requires further investigations

- Finger test: ↓Bleeding/”dishwater pus”/lack of resistance to blunt dissection post 2cm incision positive findings

- CT/ MRI helpful in ambiguous cases

6. Any patient with a LRINEC score of 6 requires further investigations for NF

- Quick algorithm listed here


website re-design

I am contemplating on re-designing the website a little to make it more 'user-friendly' on the front and back end, especialy on mobile devices.  Unfortunately, that means there would be a few changes in the ways we can access the website. 'User-friendly' usually means complex programs and software running in the background, all of which do not play nice with the arachiac versions of windows Internet Explorer, the web browser of choice on all HNEH computers.   Before I bite the bullet and go ahead, I am interested to hear many of your opinions on the matter and whether there is anything more or less you would like on our department website.  PLEASE, fill out this short survey and/or comment to this post.


Create your free online surveys with SurveyMonkey , the world's leading questionnaire tool.



Journal club: Transfusion strategies for acute upper GI bleeding

The study: in 921 patients with severe acute upper GI bleeeding, 461 were randomally assigned to a restrictive strategy (transfusion when Hb < 7 g/dL) & 460 were randomally assigned to a liberal strategy (transfusion when Hb < 9g/dL).


Result: In patients with severe acute upper gastrointestinal bleeding the outcomes were significantly improved with a restrictive transfusion strategy (Threshold < 7 g/dL). The restrictive group received significantly less transfusions. This resulted in a reduction in cost & use of blood. The restrictive group had a lower mortality, rebleeding & complication rate.


BOTTOM LINE: Having a transfusion threshold of < 7g/dL appears to have increased benefit, reduced harms & reduced costs. It appears to be a safe option for managing haemdynamically stable patients with upper GIH who are not exsanguinating. (It is important to note that patients with acute coronary syndrome, transient ischaemic attack, stroke and symptomatic peripheral vasculopathy were excluded from this study & therefore need to be considered for a more liberal transfusion strategy.)


Link to the full article


Link to the full review


Journal club: ARDS NET trial

As part of the project for our educational term, Mick Sales and I are going to be putting some regular journal article reviews on the site.

We will be using the CASP UK critical appraisal skill proforma to help us analyse these articles…but neither of us are EBM experts and so if you disagree with our review please post in the comments and let us know!

Most of the articles will be taken from the 52 landmark article post in ALiEM previously bought up by Tim Cowan.

The first study I have reviewed is the ARDS NET study of low tidal volume ventilation.

The link to the article and the appraisal tools used are listed here.

The ARDs NET ventilator protocol is here.

For those interested in the full review the link is here

Bottom line:

Lower tidal volume ventilation has a mortality benefit in patients with ARDS (8%), with a NNT of 12.5.

This has led to changes in ventilator strategies for all patients with TV of 6-8mls/kg recommended.

As a result of this study a protocolised ventilator protocol to meet oxygenation goals by titrating FiO2 and PEEP in ARDS patients has also been widely adopted.

Massive article!

Cheers - Dave


Serotonin syndrome/toxicity and NMS

Dear All,

Further to my talk this morning a couple of links :

A very good review of serotonin syndrome/toxicity here

A 'Practice' article from early 2014 in BMJ here

The original study deriving the Hunter criteria for serotonin toxicity here

Monograph on serotonin syndrome including comparison with neuroleptic malignant syndrome here




Cardiac catastrophe

Challenging case that I was previously involved with.....

Gentleman in his 40’s, referred from local ECHO provider due to severe cardiac failure and tachy-arrhythmia.

On initial assessment the patient is noted to be markedly diaphoretic, tachypneic (RR 28) and tachycardic (172bpm) with a marginal blood pressure (100/60).

He is saturating well on room air, does not feel SOB at present but notes a markedly limited exercise tolerance and has pedal oedema to his knees with a delayed capillary refill (4 secs).

A brief history is taken while IV access/ECG’s are obtained which reveals that the patient had been previously well, with no significant past medical history or regular medications.

His issue had began a few months ago when he had developed a persistent cough which was worse at night without any infective features.

Had been subsequently treated with multiple courses of antibiotics and steroids for a presumed infective exacerbation of previously undiagnosed COPD, and in the last week had deteriorated markedly to the extent where he was unable to walk more than a few metres.

An ECHO had been booked on the day of presentation which showed severe global hypokinesis of both R and LV with a LVEF of 10%

His initial investigations are listed below:

-       ECG

-        CXR

-        Venous gas

A review of his previous notes found an old ECG with a pre-existing LBBB.

How would you want to manage this patient?!

Will post next week with the patients progress…


ACEM Vimeo channel

Worth a look:



HS Troponin follow up

So I was following up recently on my patient with the elevated troponin and it looks like I may have made a mistake.

On review of Auslab, it appears that the result of 160 that I thought came from the patients 2nd test was actually the lab re-spinning the initial sample.

His actual retest result was <9.


By the time I learnt all this though, the case had really spiked my curiosity in HS troponin, and in particular how I should be dealing with it on the floor.

So what I thought I’d do in this post, is give a brief summary of the article that JP attached for those who hadn’t had a chance to read it, and then outline the best resource I’ve found so far as to how we should be using the HS troponin in ED.

 JP’s article: Reference 1

Methods: Study was part of the APACE trial, and >2000 patients presenting to ED with chest pain (onset or peak in the last 6-12 hours) were consecutively enrolled.

Based on my (very limited) ability in literature appraisal, it appeared to be a pretty good study with generalizable results.

Patients had standard troponin measurements taken as well as HS troponins measured at 1/2/3 and 6hrs post arrival.

The patients were deemed to have ACS if they had elevated troponins, rise or fall in the troponin level (using 30% of the reference range) combined with signs of ischaemia (ECG/history)

The final diagnosis was made by cardiologist who had access to all the patients’ investigations during the next 90 days (including Angio/EST/ECHO etc.)

 The interesting thing about the study was that it tested results and calculated the Sn/Sp for the four main HS troponin assays and so I will focus on talking about the assay that we use locally (Abbott)

 Sensitivities/specificities (and NPV/PPV) for the Abbott assay were:

-          Presenting >6hrs post symptoms: Sn 84%/NPV 96. Sp 90 and PPV 76% (table 2)

-          <3 hours: Sn 50%/NPV 89. Sp 97% and PPV of 85

One of the real interesting things about this study (and the big change in the diagnostic guidelines for ACS) was that a one off elevated troponin is not enough to rule in or out ACS. You need to do serial sampling on all patients.

The European Society of Cardiology has published a review article about this which I found very helpful in terms of using HS troponin, and in particular when describing the delta (the change in troponin levels) of troponin required to diagnose ACS.

Please see the link here.

The big points from this article were:

  1. Diagnosis of ACS requires:

-          Troponin above the reference range coupled with a significant delta

-          Signs of ischaemia (ECG or history)

The flow chart they recommended for the diagnosis of ACS is below


  1. Diagnose myocardial necrosis with either

-          Initial troponin >upper reference limit (URL) with a subsequent increase of >20% of initial value

-          Initial troponin below the URL when the repeat test is >the URL due to an increase of >50% URL

To describe that using our URL for males (26) a positive result could occur with either:

-          Initial troponin of 30 with repeat testing of >36

-          Initial troponin of 20 with repeat levels at >33 (Increase of >13 which is >50% URL)

 I couldn't find any reference here to fall in troponin levels but as per JP's comments in the previous post that is also talked about in the literature.

 2. History or ECG that is suggestive of ischaemia then = ACS


Bottom Line:

-          One off HS troponin results are not sufficient to rule in ACS

-          Need to check the delta in all patients where ACS is suspected

-          HS troponin is very specific for myocardial necrosis but not for ACS

-          The Sensitivity and specificity of our local assay are not as good as I would have thought.


Anyone else’s heads a bit sore?!




  1. Hoeller R et al, 2013, ‘Normal presenting levels of high-sensitivity troponin and myocardial infarction’, Heart, 0:1-6
  2. Thygesen K et al, 2012, ‘How to use high sensitivity cardiac troponins in acute cardiac care, European Heart Journal, 33, 2252-2257

Are you sure you want me to see this patient?!

The case:

52 year old man presenting with a 5/7 history of diffuse lower abdominal pain

He had been febrile for 3/7, had some nausea and vomiting and had not opened his bowels for 5/7.

He was otherwise well with no regular medications or past medical history

On examination he was febrile to 39 degrees celcius, tachycardic at 108 bpm with a peritonitic abdomen.

Surgeons were consulted and a CT scan organised.

Bloods had been taken before I reviewed the patient and were pending.

Prior to the CT scan the surgical registrar arrived to review the patient and had a look at the bloods which included a high sensitivity troponin (?!)

Unfortunately, this was elevated at 461, prompting the question above.

I was quite surprised by this reading and went back to reassess the patient.

He denied any chest pain, and was very fit and active with a good exercise tolerance and no risk factors.

Serial ECG's were performed (normal) and a repeat troponin was taken which was still elevated at 161.

The on call cardiologist was then consulted who advised that this was a false positive test and that we should disregard the troponin.

Like most of us I am still trying to get my head around the new HS troponin assays.

I was lucky enough to attend the SMACC conference this year and heard Louise Cullen and Rick Body speak on this issue.

They were both of the opinion that the HS troponin is very specific for heart damage (and shouldn't be raised at all if the heart is not affected) and if there were elevations it was due to an insult of some sort (though not necessarily ischaemia).

Based on that logic it would seem that the patient must have had a type 2 myocardial infarction....but I'm still quite sceptical that this occured in the patient given how fit and healthy he normally was.

Would be very keen to hear others thoughts and in particular if they had any information on this issue!

The patient subsequently had a CT that showed a perforated appendiceal abscess and went to OT where he was found to have 4 quadrant peritonitis with multiple adhesions.

He was discharged 6 days later and has been fine since.


TAPNA 2014

G'day All,

On April 30th till 3rd May Newcastle will once again host the Toxicology And Poisons Network Australasia, TAPNA, scientific meeting. The plenary sessions will include talks on marine poisoning, the latest in redback envenoming following the RAVE II trial and a session on addiction medicine. Go to www.tapna.net for information. 

On Saturday 3rd May we will be running a one day Toxicology workshop aimed at ED/acute care trainees, final programme will be on the website within the next week. Early bird price is $250.00 Hoping a few of you can make it. This is the weekend of the fellowship clinicals so obviously those involved in that won't be coming but everyone else !!!

Finally, the slideshare website through which I put up some of last year's talks as well as Sam Vidler's presentation from last year, is going to discontinue the slidecast service soon. This means that after April you won't be able to access any of the audio-visual presentations. I am hoping to have these (and some more talks) up on a different platform soon.