WBA Update

Hi all,


WBA (work based assessments) for all advanced/provisional trainees is on from next year!!! It’s not a trial anymore; going live on 2nd Feb 2015. Preparations are underway for smooth takeoff; check this location for more updates.

Meanwhile look at ACEM website for more information…

More soon



Steve Walker’s Update: Tranexamic Acid in Trauma.



Epistaxis and Tranexamic acid

A new and rapid method for epistaxis treatment using injectable form of tranexamic acid topically: a randomized controlled trial.

Author: Zahed R, Moharamzadeh P, Alizadeharasi S, Ghasemi A, Saeedi M.

Reference: Am J Emerg Med. 2013 Sep;31(9):1389-92. doi: 10.1016/j.ajem.2013.06.043. Epub 2013 Jul 30.

Summary: This randomised controlled trial compared tranexamic acid with anterior nasal packing for patients with anterior epistaxis presenting to ED. 216 subjects with epistaxis were randomised to the injectable form of tranexamic acid (500 mg in 5 ml) applied topically, or anterior nasal packing with pledgets coated with tetracycline ointment. Outcome measures were time to cessation of bleeding, length of hospital stay (hours), and re-bleeding rates at 24 hours and 1 week. Patient satisfaction with treatment was rated on a 1-10 scale. Tranexamic acid was superior to anterior nasal packing for arresting bleeding at 10 minutes; 71 vs. 31.2% respectively (OR 2.28, 95% CI 1.68-3.09, p < 0.001) and discharge within 2 hours; 95.3 vs. 6.4% (p < 0.001). No difference was observed in between-group rates of re-bleeding at 24 hours; 4.7 vs. 11% (p = 0.128). Patient satisfaction with treatment was significantly greater for tranexamic acid compared to anterior nasal packing; 8.5 vs. 4.4 (p < 0.001).

Comment: The study showed good results, control of bleeding within 10 mins (71%) and discharged within 2hours(95%). More studies required for confirmation.



The workup for a possible SAH is a topic of much interest to ED doctors. The problem is the condition is fairly rare, the potential consequences of a missed SAH are devastating, and the workup remains problematic.

The LP in particular is a cause of much angst. Most patients are apprehensive about the procedure. It is time consuming, and can be technically difficult in some patients (especially the obese). There are frequent false positives – up to 20% (depending on RBC cut-off used). Spectrophotometry is advocated to help sort out these false positives. This however brings its own problems – spectrophotometry is not universally available, and differentiation between fresh blood (traumatic LP) and older blood (SAH) necessitates a 12 hour delay to do the LP.

Given all this, it is fair to say a patient awaiting a CT for a possible SAH is not the most popular handover!

There are 4 conditions we need to consider

  1. An incidental aneurysm. It is estimated that 4-6 % of the population have an intra-cranial aneurysm. Fortunately the vast majority of these will never cause problems and (as with prostate cancer), far more people will die with an aneurysm than will die because of the aneurysm.
  2. A symptomatic enlarging aneurysm which has not ruptured. This can be a cause of a headache, or occasionally a cranial nerve palsy (classically 3rd nerve). We want to find these as we believe a painful (enlarging) aneurysm is at significantly increased short term risk of rupturing – as with a painful enlarging AAA.
  3. An aneurysm which has ruptured and caused a SAH. This is the one we all think about. Some people are lucky and get a small warning bleed prior to a second larger bleed. We definitely want to catch this group. Large bleeds have a high mortality, and there is a high risk of permanent neurological damage if it is not fatal.
  4. A non-aneurysmal SAH. That is, a SAH arising from an angiographically normal artery. These can present like an aneurysmal SAH, with a sudden severe headache. However there is not much we can do about these bleeds – we can’t find the bleeding point, and we can hardly go around clipping off normal Circle of Willis arteries. Fortunately this condition has a better natural history and more benign long term prognosis than aneurysmal haemorrhages.

So we definitely want to diagnose 2 and 3. These are the conditions a neurosurgeon (or interventional radiologist) can intervene to change short term outlook.

It is probably helpful to know about 1 and 4. The patient can be advised they have an aneurysm or a bleed, they can be counselled to stop smoking, and hypertension (and other vascular risk factors) can be closely managed.

But the question we want to ask is “Does the patient have an aneurysm which has either bled, or which might bleed in the near future, and which is amenable to intervention?” This is the real question underlying our workup for ? SAH.

Prior to CT, the only way of diagnosing an aneurysm was by conventional angiography. This procedure has always carried significant morbidity and even mortality, and therefore was not a procedure to be undertaken lightly. LP was therefore used to risk stratify the patient. If there was no bleed, then it was not appropriate to expose the patient to the hazards of angiography. Only if there was a SAH was the risk of angiography justified. So we looked for the bleed to help decide if we wanted to look for the aneurysm.

Early generation CT scanners changed this a bit. They were good enough to find a large bleed, and were sometimes able to see a small bleed. They were not good enough to reliably find the aneurysm – especially if IV contrast was not used. So the rationale for CT was to find a bleed (rather than an aneurysm).  In addition, CT sometimes found another diagnosis (tumor, intra-cerebral bleed), and also helped exclude a space occupying lesion that would preclude LP. Because early CT missed small SAH, LP remained entrenched as part of the ED workup. So the algorithm then became CT, LP if CT negative, and then angiography if LP positive. From an ED perspective, the job was still to find a bleed, and admit the patient under someone who would go looking for an aneurysm. And so the ED literature is focused on the hemorrhage rather than the aneurysm.

Newer generation CT’s are much better at finding small bleeds. One large study has suggested the sensitivity is 100% within 6 hours of the bleed. If a patient presents with a headache within 6 hours and a good quality CT is performed and is read as normal by an experienced radiologist, then you are done. No LP. Some people are less confident that the sensitivity can be 100%. But most people agree it is pretty close and the need for a LP today is much reduced. Note you are still left doing an LP if the CT is performed more than 6 hours after headache onset.

So right now, most of us are doing a CT and doing this ASAP, and sometimes doing a delayed (12 hour) LP to sort out delayed presentations or perhaps a particularly high risk history. I think that is the state of play at present. Again, we are more intent on finding the bleed than the aneurysm.

However I suspect there is another chapter to be written in this story. The aneurysm (including a high risk non-ruptured aneurysm) is more important than the bleed itself. At present, our focus is perhaps too much on the bleed and not enough on the aneurysm. The original intent of the LP was to screen which patients underwent angiography. But the question the neurosurgeons always wanted to answer was about finding an aneurysm they could do something about, not finding the blood per se.

With current CT, we now have the option of going after the aneurysm. CT angiography has similar sensitivity to conventional angiography, is quick, and is non-invasive. So should we just do the CT and CT angiography for all SAH workup? If there is no aneurysm, then maybe you are done. Perhaps there is little point doing a LP looking for a bleed if there is nothing to be done (or that can be done) for it. The neurosurgeon (interventional radiologist) can do nothing for a non-aneurysmal bleed. They can only do something about an aneurysm.

There are pros and cons to such an approach:


  1. No more LPs. No more admitting patients to EMU for someone else to do an LP the next day. Even if the story is good. Even if the headache was 8 hours ago. If there is no aneurysm, then it doesn’t matter.
  2. Quick and easy. The patients will like it. Busy EDs will like it.
  3. If the patient has an aneurysm, it is probably worth knowing about. Stop smoking. Watch your BP. And do come to hospital quickly if you ever get a really bad headache.
  4. It is easier for us to manage the 5% of patients with a real (but incidental) aneurysm than the 20% with a traumatic LP.
  5. May find other conditions. We have had a missed carotid dissection in a 30ish year old female. She did badly. Her CT was normal. However a CT angiography may have found this.
  6. The small population of patients who present repeatedly with high risk sounding headaches don’t require comprehensive evaluation for a SAH each time. If they didn’t have an aneurysm 2 months ago, they don’t have an important SAH (that we can do something about) today.


  1. Need for IV contrast. This is not usually an issue as we are mostly looking at middle aged (rather than elderly) patients. However it will sometimes be a factor (especially with increased rates of diabetes in this population)
  2. Increased radiation. A 2nd scan with contrast after an initial non-contrast scan. Again, this is probably not a huge problem in the middle aged, but will be important in younger patients.
  3. The biggest concern may be labelling 5% or so of patients as having an aneurysm. It is probably some patients will be made anxious about being told they have an aneurysm. This knowledge may have implications for certain occupations (e.g. pilots), and also for life insurance or travel insurance (given the “duty to disclose” obligations of these policies).

On balance, I suspect this is the way we will go. Patients want a quick answer with minimum short term risk and discomfort. Doctors want quick answers, and want to be safe from medico legal risk.

With ongoing advances in CT, with increased availability of MRI and MRA, with EDs struggling with increased patient numbers, and with the increasing need to sort things out as efficiently as possible, I think all the drivers will push this in one direction only.

To people with a different view about this, I offer the following 5 letters. CT KUB.

Dr Steve Walker, Staff Specialist, Nepean Emergency Department.



Quite a few months back I was supervising a registrar intubating a patient using the C-MAC. The patient was a middle aged male who had a decreased conscious state following an OD. Apart from being somewhat overweight, there were no predictors of a difficult intubation.

Preparation and pre-oxygenation were all standard. However intubation was initially unsuccessful. The C-MAC screen showed a good (great) view of the larynx, but the registrar was unable to bring the tip of the tube into the field of view, and the tube passed down the esophagus each time it was (blindly) advanced. Attempts to intubate were ceased after the patient began to desaturate. He was easily ventilated with a bag and mask, his saturations promptly normalized, and there was no adverse outcome. So no real problem. I subsequently intubated the patient with a conventional laryngoscope, which provided a grade 1 view.

Later that evening I was having a coffee with the registrar. We tried to work out how the C-MAC had turned a grade 1 view into a patient unable to be intubated. Bearing in mind that the C-MAC is claimed to make intubation safer and easier, is promoted as an invaluable teaching tool, and some advocates claim it is now “standard of care” and predict the end of conventional laryngoscopy.

It struck me that conventional laryngoscopy is a sequential left hand and then right hand skill:

  1. You use your left hand to insert the laryngoscope and then manipulate the blade in order to provide a good view. Sure you might extend the head or externally manipulate the larynx with your right hand. But it is primarily a left hand task. Once you have a good view, you often relax a bit. Nothing can go wrong now. Just keep that view.
  2. The act of passing a tube (or bougie) using your right hand – while keeping your left hand still so as to maintain your view.

I believe this is almost a subconscious process reinforced over the years. Get a view with your left hand, keep your left hand perfectly still, and then intubate the patient. Simple.

If you use the C-MAC as a conventional scope (ie you use direct vision to look down the mouth and don’t look at the screen), then the above still holds.

If however you look at the screen, the above all changes – possibly without you recognising it.

The C-MAC is designed to create a good view. And it does this very well. You can pretty much insert it however you want, and you will get a good view of the larynx. As seen from the lens on the blade. This may however be very different from the view you would see looking down the patients mouth – which is the path the tube has to follow. You may have a grade 1 view as seen from behind the patients tongue, but a grade 4 view using direct vision.

So now you have got a great view on the screen. Except there is now a disconnect between what you are seeing on the screen, and what happens next. You never see the tube appear on the screen. However because you still have a great view, you don’t realise you need to manipulate the blade to provide a clear path for the tube. Subconsciously, the path must be fine (and thus nothing for the left hand to do) as the view is good. I think this is what happened in this case.

I subsequently spoke to a couple of anaesthetic colleagues. They confirmed this is what most likely happened, although one explained it a little differently as “failure to control the tongue.” We have all been taught to go down the right side of the tongue and to sweep / lift it out of the way in order to obtain a clear view. You have to control the tongue. However you can skip this step using the C-MAC screen – the screen effectively puts you somewhere behind the base of the tongue and so you don’t have to control it. You have a good view even if the airway superior to the lens is obstructed by the tongue. If the tongue has fallen against the posterior pharyngeal wall, it will helpfully guide an advancing tube into the esophagus.

These anaesthetists confirmed the accepted practice when using the C-MAC is for the intubator to use direct vision. The screen is for other people to watch. The intubator not only has to have a view of the larynx, but needs to have a clear view of the entire path the tube needs to follow.


So with that long preamble, I think there is a broader issue here. New technology and new devices can certainly help us to our jobs better than before. No doubt about that. But as with this case, it can also introduce new problems or risks or traps. And these are not always immediately obvious.

The salespeople promoting the technology have an incentive to talk up the positives, rather than pointing out the potential problems (and in all fairness they may not be aware of the problems – how many C-MAC salespeople intubate patients?) And even well meaning colleagues enthusiastic about some new device (and with no commercial conflict of interest) may gloss over the dangers – perhaps because they are so obvious to them they don’t require discussion. One anaesthetist was puzzled why the registrar was ever looking at the screen in the first place – “But everyone knows you need to use it like a conventional scope.” I guess someone forgot to tell the registrar and myself.

So we need to know how to use new devices and new technology safely. This means we need to understand how it actually works, the subtle ways it can change things, and we need to be aware of the hazards and traps.

Dr Steve Walker, Staff Specialist, Nepean Emergency Department.

Mathematical Truisms to help when your brain is stretched

This is from the July issue of Annals – a light hearted review of some useful clinical formulas. Enjoy.

Mathematical Truisms in EM Goodman Annals EM 2013

Airway management in obesity

This article from Stuart relates to our recent M&M case of an obese patient with respiratory failure

Airway management in bariatric patients Annals 2010

Two nice articles from EMA (if you don’t get it or don’t read it)

Metoclopromide and DIA EMA 2013

Diagnostic utility of VE EMA 2013

I have added two articles from June EMA. Both are neat little studies with good methodology and a simple bottom line. The first challenges the belief that that bolus metoclopromide is associated with akathisia. The second that vaginal examination helps in 1st trimester bleeding. In this study, clinical assessment was correct in only half the cases and did not correctly diagnose ectopic pregnancy at all. None of the six cases diagnosed as ectopic, had an ectopic and none of the four who had an ectopic were diagnosed clinically. VE made no difference. A good argument for bedside ultrasound.

Another Interesting Resource

The Royal College of Pathologists Australasia, has come up with this website, which summaries the pathology tests needed for various clinical problems. This is not only helpful in doing the relevant tests but also to avoid doing unnecessary tests. There are useful summary of signs and symptoms for various diseases and also few pathology decision tool. Worth having a look.
Click this link

Pearls from Emergency Medicine Abstracts 2013

EMA Pearls June 2013

Pearls this year’s Emergency Medicine Abstracts Course June 2013. Author: Colin Xavier

And Steve Walker’s take on the course:

S.Walker Emergency Medical Abstracts June 2013 Report


Two new articles posted

I have posted a couple of new articles

WCC, CRP & PCT remain tests we love ordering, but recent systematic reviews show they have a limited ability to identify serious infection over and above our clinical assessment. The attached editorial gives a balanced assessment.

The second article again shows the risks of ICH in patients who sustain a minor head injury whilst on clopidogrel. A liberal use of CT is recommended.


Clopidogrel in Minor Head Injury

Risk of ICH in Patients on Clopidogrel

Another article on the risks of ICH in patients on Clopidogrel (10% risk) and Warfarin (4% risk) who sustain a minor head injury. The authors could not identify a low risk group, so recommend liberal use of CT in all these patients, even if assymptomatic.


PCT & CRP Moran Editorial Annals EM 2012

PCT & CRP Yo Annals EM 2012

For those of you who attended the recent Paediatric day at CHW, there was discussion of the value of CPR and PCT. The articles above are one of the ones referenced from Annals of Emergency Medicine and the accompanying editorial. Neither have strong enough LRs to be game changers in a febrile child.

A Clinician’s Guide to Australian Venomous Bites and Stings

BioCSL has released A Clinician’s Guide to Australian Venomous Bites and Stings: incorporating the updated CSL Antivenom Handbook, designed to educate and provide emergency reference material to doctors.
Author – Professor Julian White.

All medical professionals can a get a free copy of the handbook by emailing [email protected] and providing their postal address and AHPRA number. Free copy of the book will be posted to your home address.

Book worth reading.


Bougie assisted surgical cricothyroidotomy

An excellent short video on how to perform a surgical cricothyroidotomy, utilising a bougie to ensure to you are in the trachea. Any questions or comments, let me know.





I bumped my foot…oops!!

62 yrs male, Poorly controlled diabetes with peripheral vascular disease. Hx of trivial injury to R foot 3 days prior to presentation. In ED, HR 89/mt, BP 124/76, Temp 38.7C. BSL 16.2, Ketones 2.5, WCC 24.5, CPR 499, PCT 8.71. On examination of foot, swollen, blister over dorsum of foot, erythematous, tender. Xrays ordered to look for osteomyelitis; comment on the lateral foot xray.


CMAC versus direct laryngoscopy

CMAC versus Direct Laryngoscopy Sakles Ann EM 2012

A timely article about CMAC as we are about to introduce it at Nepean


Blackouts and Syncope

Nice video to brush up on this important/ common situation we face almost everyday…. This video is created by an EM trainee at Ireland, Dr Andy Neil.
Please click here for the video.

Credit: Dr Andy Neil.

Nurse Education Up & Running

The Nursing Education section of finally has some content. Of interest to all staff is a list of the Mandatory Training that all NBMLHD employees need to complete. There are also some really good external educational links for all ED staff.

World Sepsis Day

World Sepsis Day – 13 September 2012!

  Recognise  Resuscitate  Refer

 See a funny Sepsis “rap”

Ring Removal using Oxygen Mask Strap

This technique is not new to the world; we have used this technique for ring removal with a suture material or wire with some success. Check out this nifty trick on ring removal by Dr. Simon Carley (Centre For Evidence Based Emergency Care at Manchester Metropolitan University) using Oxygen Mask Strap. Try it out next time.


aVR – Gets no respect

Watch this interesting video by the influential Dr Amal Mattu. This would change your views about aVR.

Click here to watch the video

Right-Sizing Testing for PE

A thoughtful editorial on  the approach to testing low risk PE patients. It argues that any testing (even D’dimer) for PERC negative patients does more harm than good.


 Right Sizing Testing for PE Green & Yealy Annals EM 2012

Intracranial Haemorrhage in Patients on Anticoagulation

This prospective study of patients with blunt head trauma showed that patients on clopidogrel had a higher rate of intracranial haemorrhage (12%) than those on Warfarin (5%), but warfarin had a small rate (0.6%) of delayed haemorrhage.  In this study, 97 % of patients were mild head injury with only 18% having a history of loss of consciousness or amnesia. The implication is that like patients on warfarin, you should have a very low threshhold for scanning patients on clopidogrel.

 Intracranial Haemorrhage with Anticoagulants Annals EM 2012


Locked knee

10 yr old female presented to ED with painful swollen knee after a fall, while playing netball. On examination, unable to flex or extend the knee. What do you think is the cause for her locked knee? What is your management plan?

EMSS GO-LIVE 28 August 2012

EMSS Go-Live 28 August 2012

[ujicountdown id=”Countdown to Go-Live” expire=”2012/08/28 00:00″ hide = “true”] 


Registrars/ CMOs roster update

New roster for the month of August to October 2012 has been uploaded under “Medical Roster” section in our website.

Contrast Induced Nephropathy with CTPA

An interesting article in light of our recent journal club looking at the use of NAC to prevent CIN. The article shows more patients suffered CIN than were found to have PE. The PE story only gets murkier.

CIN following CTPA AEM 2012


This patient presented with syncope. What are the abnormalities on the ECG?



Answer:[expand title=”Open” swaptitle=”Close”]

•Sinus bradycardia
•RBBB block (note RSR’ V1-V4 with associated repolarisation abnormality and S wave in V6)
•LAHB with marked left axis deviation

These findings raise the possibility of a transient high degree AV block causing the syncope.[/expand]

Missed more often, than it is recognized…

A 50 year old man presents following a fall down some stairs. He landed on his left elbow. He complains of pain in the left shoulder. On examination, he is unable to move his L shoulder. There is swelling and pain in the region of the left shoulder. No open wound noted.

What do these Xrays of his left shoulder show, and how would you treat it?

Answer: [expand title=”Open” swaptitle=”Close”] The AP film demonstrates a classic “light bulb sign” of a posterior glenohumeral dislocation (the humeral head appears atypically rounded compared to usual). The lateral glenoid “Y” view confirms posterior dislocation of the humeral head (the humeral head is posterior to the “Y” formed by the lateral view of the scapula). An axillary view of the shoulder should be used for additional confirmation, but was not done in this case. Because the changes are subtle, posterior shoulder dislocation is often diagnosed late.

Closed reduction is considered appropriate if the dislocation is reasonably acute (within 3-6 weeks) and if any resultant defect in the humeral head is small (less than 25 % of articular surface, best judged on axillary view).

Reduction of a posterior shoulder dislocation is generally considered more difficult than reducing an anterior dislocation. Good procedural sedation will facilitate this. However, sometimes a GA in theatre will be required.

The arm will be adducted and internally rotated. Traction is applied longitudinally with the elbow in 90 degree flexion. The humeral head is disengaged from the posterior glenoid, and then the arm is externally rotated, which should reduce the dislocation, and result in a return of mobility.

The humeral head can be disengaged directly, by getting an assistant to apply pressure to the humeral head; or indirectly, by applying lateral pressure to the medial side of the upper humerus (thereby moving the humeral head laterally and increasing the adducted position of the elbow). Once the humeral head is disengaged, it should be possible to externally rotate the still adducted arm. However, the external rotation needs to be done carefully as the humeral head can fracture if it has not been disengaged from the glenoid.

Successful reduction should be signalled by a clunk and return of mobility.

A triple set of Xrays (AP, lateral and axillary) should be obtained post reduction to avoid missing any persisting dislocation. If in doubt a CT may be required. The arm requires a sling for three weeks. Orthopaedic referral is mandatory.
Natalie Vu

EMA Podcast June 2012































Spot diagnosis 4

What is the diagnosis? What is the name of test a and test b?

(please use the “Leave a reply” section below to post your response)


What is the cause for these changes in teeth?

Look at my neck…

60 yr old female presented to ED for headache. On examination HR 110/mt, BP 188/102mmHg. Also noticed this interesting finding in the neck,

What do you think is the likely cause? What is the differential diagnosis?

Light Box #2

32 years old male presented to ED for first episode of witnessed seizure. Hx of constant headache for 3 weeks, unwell feeling. Recently migrated to Australia from Mexico. No hx of seizures before. Nil other medical problems. CT scan preformed showed the following. What is the likely diagnosis?


Blood Gas Trivia #1

[box]28 yrs old man, BIBA for decreased level of consciousness. Given oxygen enroute to hospital by paramedics. Blood gas done on arrival showed,

pH 6.87 ( 7.35-7.45)

PO2 204 (75 – 100)

PCO2 16 ( 35-45)

HCO3 4 ( 22-26)

BE -29

Lactate 3.1

Half an hour later we received the following blood test results,

Na 140, K 4.9, Cl 99, Urea 20.2, Creat 224, LFTs – unremarkable, BSL 75.1, CRP 4, Hb 95, WCC 36.1, Plat 407, Neu 32.1

Can you describe and interpret the results? What is the differential diagnosis?

( Please use the “Leave a Reply” area to answer. Feel free to attempt; as answers will be kept confidential, only correct answer(s) will be published online.We expect a response from all advanced trainees)


ECG: What would you do next?

A 45 year old man presented with shortness and breath and mild chest discomfort. This is his ECG. He is on haemodialysis for renal failure and is known to have aortic stenosis.

Which of the following is/are the most appropriate response(s)?

a)    Activate the STEMI page

b)   Check his electolytes

c)    Repeat the ECG in 15 minutes

d)   Ask for an urgent transthoracic echo

e)    Burst into tears because clinical medicine is too hard


ANSWER:[expand title=”open” swaptitle=”close”] [box] b, c and possibly e

This man had aortic stenosis and renal failure, his potassium was 6.7.
The worrying feature of this ECG is ST elevation in V2 and V3 – note that the segments are concave and that there are deep S waves in the praecordial leads consistent with LV hypertrophy. It is a rule that the deeper the S wave the greater the ST elevation. LV hypertrophy is one of the conditions most frequently confused with acute MI.
About 90% of young otherwise healthy men have ST elevation of between 1 and 3 mm in the anterior praecordial leads – “early repolarisation”.
Hyperkalaemia is another well-recognised cause of ST elevation.
In this case, his symptoms were not consistent with an acute MI and the most appropriate response is to repeat the ECG in fifteen minutes to look for evolving changes and to check his electrolytes. Answer e reflects the shortcomings of ECGs as a tool and the daily frustrations we face in clinical assessment, however, bursting into tears is unlikely to be helpful.

Other causes of ST elevation other than AMI are:
–       LBBB
–       Acute pericarditis and myocarditis
–       Burgada syndrome
–       Pulmonary embolism
–       Transthoracic cardioversion
–       Prinzmetal’s angina

For a good discussion of causes of ST elevation see: Wang K, NEJM 2003; 349:2128-35

Syncope, otherwise normal….

32 yrs old female, presented to ED for one episode of fainting, witnessed by husband. Loss of consciousness few seconds. No hx of headache or chest pain associated with syncope. No previous syncopal episodes, but had few episodes of self resolved palpitations, not investigated further. On examination, vitals stable, looked well. Blood results were unremarkable. This is her ECG; What do you think is the problem? What is the pathophysiology? What is the definitive treatment? (Please use the “Leave a reply”  section below to post your answer)

Unusual presentation….

An otherwise well 60 year old man, DC, presents with palpitations whilst out walking three hours ago.  He admits to mild chest tightness.  He denies any history of fever, cough, chest pain or breathlessness.  A 12 lead ECG is taken and is as below.  What is the rhythm?  How can you be sure? How will you treat it?








(Click on the image to enlarge)

What happened next? [expand title=”Open” swaptitle=”Close”]

DC continues to feel palpitations and mild chest tightness.  He is given oxygen and put into Resuscitation, where 6mg of IV adenosine via  a cannula in his cubital fossa confirms that he is in atrial flutter.  His chest tightness persists despite oxygen and half an anginine.  His BP is 100/65.  As he has eaten recently but has only been in atrial flutter for a few hours, he is sedated with ketamine and cardioverted to sinus rhythm with 50 joules.











TRACK 03: 

TRACK 04: 































This rash on a teenage boy’s palms began on his hands and spread to his torso and upper and lower extremities over several days. He had no pain or pruritus. Two weeks before the lesions appeared, he had experienced fatigue, fever, and myalgia of 1 week’s duration.

The patient denied use of new skin products, detergents, or medications. He had no pets. There was no history of recent travel, and the patient was not aware of any arthropod bites. None of his family members had a similar rash. The patient was sexually active and had had 3 partners in the past 2 years; he said he always used condoms. His history was otherwise unremarkable, as were physical findings.

What is the likely cause? what are the differential diagnosis? (Please use the “Leave a reply” section below to answer the questions)

Light Box

How good is your Xray Vision? Chest Xray and CT Chest of this patient shows an interesting finding. What is the likely diagnosis?

(please type your response in the “Leave a reply” area  below. Correct answer will be published once enough replies are received)


Dangerous sign

[box]An 80 year old male with a past history of hypertension, high cholesterol, 50 pack years smoking, and bilateral fem-pop bypasses presents dehydrated and very weak.  His ECG is as shown below. What is your diagnosis?

ECG repeated few hours later showed,[expand title=”Open” swaptitle=”Close”]

[/expand] Luckily we have received the patients blood test results; can you interpret and confirm your diagnosis?[expand title=”Open” swaptitle=”Close”]



Answer [expand title=”Open” swaptitle=”Close”] You are right. Its case of acute renal failure with severe hyperkalemia. The first ECG sign of hyperkalaemia is peaked T waves and usually appears once K level is at 6 mmol/L.

Second sign is prolongation of PR interval which can be seen with K level going around or above 7 mmol/L.

Absent P wave with widen QRS complex is the third manifestation and is a very dangerous sign. It means that atrial activity is lost and stage is set for ventricular tachycardia/fibrillation. It is usually seen at level around 8-9 mol/L

At this point the patient becomes  paralysed by weakness and can have respiratory arrest and then Ventricular tachycardia/fibrillation is the price you pay for ignoring above changes on monitor.

See Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration (source: Emerg Med J 2002; 19:74-77)

Post by : Dr Shane Trevithick[/expand][/box]



What is your diagnosis? Use the comment/reply link below to answer.

(correct answer will be published once enough replies are received…)

Xray Quiz

[mtouchquiz 10]

EMA April 2012 Podcast

EMA April 2012 Audio podcast































Give it a try….

What do you think about this ECG? Can you describe and interpret? Click on the image to enlarge.
(use the comment link at the bottom to post your answers)

Anterior Epistaxis First Aid in ED

A simple trick to help you manage your epistaxis patients in the ED.
For an alternative device check out Cliff Reid’s article from 2001 here:

Recent Staffing Changes – Clarification from Dr Bishop

1. Recent Staffing Changes

Just some further discussion and clarification re the medical staffing
You may have noticed that we are now rostering a registrar to EMU/WRAC/FT. The aim of this is to give the registrars some exposure to EMU and assist the staff specialists in managing this load which is likely to increase with the 4 four target. Similarly this registrar will be the first port of call for clinical advice etc from the NPs in Fast Track. Again this gives the registrars some exposure to this case mix and allows the WRAC staff specialist to concentrate on patient flow through WRAC.
There are still some CMO shifts in Fast Track. When they are there they will obviously bethe fisrt port of call for the NPs. Also,just to clarify, the Fast Track shift times aren’t fixed to the shift times for acute care, but could be varied in conjunction with Arlene and Jayshri.
However there will be some shifts when we are short staffed on the registrar roster, and depending on workload, the FT CMO should also help out with WRAC – Jayshri may even roster this as a WRAC/FT shift.
At night, all fast track patients should be seen through WRAC – there will be no nursing staff in FT. You may ofcourse take patients into FT to use the eye room, plaster trolley etc. The oncoming night staff should start seeing patients between 2200 and 2300. Check with the evening staff specialists as to where the greatest need is. Picking up a couple of patients before the 2300 handover and getting a handle on what is waiting will help to ensure most patients are seen and have some plan before the staff specialist finish at midnight.
And yes the staff specialists are there until midnight  – the aim being that they have time after the handover to sort out issues identified at the handover, clear patients for EMU and ring VMOs as necessary, instead of having to do this at 0100 as has been the practice.
Finally we are making some more changes to WRAC including the development of an internal waiting room in Room 33 for patients to sit after their initial assessment. Tracey is developing some guidelines and we will undertake some further education etc prior to implementation in February.


Fluid Resuscitation in Trauma

Couple of articles worth reading.

The first paper is an evidence based review of fluid management of traumatic hemorrhagic shock. Take home points:

1.    How little we really know, how bad the science is, and that some conventional dogma is incorrect.

2.    In the bleeding patient, lost time is lost blood. Minimise delays (pre-hospital and in-hospital) prior to definitive control of hemorrhage. A common statement is that the best pre-hospital fluid is a bolus of diesel to the engine of the ambulance (ie get moving).

3.    Fluid choice doesn’t seem to have any significant impact on morbidity or mortality.

a.    No advantage to colloid. The best study here is SAFE, which concludes that crystalloids and colloids should be considered equivalent. There may be a minor logistic advantage to colloid in remote or military environments (when someone has to carry the IV fluids on their back).

b.    No clear advantage to either Saline or Hartmanns. Theoretical considerations favor Hartmanns, and some studies suggest that Hartmanns may be better (these studies are poor quality however).

c.    No advantage to hypertonic saline. Theoretically you would expect hypertonic saline to be of greatest benefit in head injuries (due to its ability to reduce ICP). However the best study addressing this (from Melbourne) failed to find a benefit.

4.    Trend towards using less fluid and less “resuscitation” than previously.

a.    Theoretical concerns of large volumes of IV fluid include increased bleeding due to hydrostatic disruption of hemostasis (“popping the clot”), dilution of hemoglobin (reduced oxygen transport), dilution of clotting factors and platelets (more bleeding), hypothermia (more bleeding) and tissue edema (including lung injury, pulmonary edema, and intra-abdominal compartment syndrome).

b.    The most famous study here is 1994 US study by Bickell et al. This showed significantly higher mortality in patients who got aggressive prehospital fluids. Note the setting of this study – inner-urban USA (= short prehospital times), and lots of penetrating trauma (ie big holes in big vessels). Care therefore needs to be taken extrapolating this data to all trauma patients.

c.    However minimizing fluids has become accepted practice. Our thinking now is that a patient does not immediately require fluid resuscitation if he has normal mentation (and therefore presumably normal tissue perfusion).

5.    Above all else, significant head injuries require normal BP. A single episode of hypotension doubles the mortality in head injury. In the setting of traumatic brain injury, the need to give fluids to maintain BP outweighs concerns about increased bleeding from a co-existing splenic injury.

6.    There is a trend to using more and earlier FFP and platelets in trauma resuscitation. There is a lot of evidence favoring this approach, although the studies are not perfect (mostly US military from Iraq and Afghanistan. However the believers are firm believers, and we are increasingly using FFP and platelets pre-emptively rather than waiting until clotting times become abnormal. Hospital based massive transfusion protocols recommending agreed fixed ratios of red cells:FP:platelets have been shown to be helpful in achieving this goal of early and more FFP and platelets.

7.    Tranexamic acid is definitely in following CRASH-2.


The second paper by Brohi is interesting in view of the current trend towards minimum volume fluid resuscitation. This paper is hard going unless you have a particular interest in coagulation! However the conclusion is that hypotension has been shown to induce activation of Protein C, and hence lead to anticoagulation! This happens very quickly (hence “acute”), and is frequently present by the time the patient has arrived in Emergency. This process has been termed “Acute Coagulopathy of Trauma”. This ACT appears to be more important than other traditional explanations for coagulopathy in trauma (eg dilutional, hypothermia). It seems strange that we would have a mechanism to initiate endogenous anti-coagulation when in a state of hemorrhagic shock. If there is an evolutionary rationale for this, it presumably lies in avoiding widespread sludging, thrombosis and ischemia when in a low perfusion state.

So we seem to be saying that excessive fluids can increase bleeding, and that insufficient fluids and uncorrected shock can induce a coagulopathy which will presumably increase bleeding. A delicate balance, especially in the early management of a seriously injured patient with lots of unknowns. What is this patients normal BP? Where is he bleeding? Does he have a significant brain injury, or is he just intoxicated?

Bottom line: Trauma is a complex entity, and we don’t know it all. Treatment decisions (including resuscitation strategy) need to be individualized taking into account the patient’s particular circumstances and competing priorities.

You can download the articles below for further reading.

Paper 1: Fluid Management in Traumatic Hemorrhagic Shock

Paper 2: Acute Coagulopathy of  Trauma (ACT)

Happy reading,

Steve Walker

Oral versus IV rehydration in gastroenteritis

Is it worth trying oral fluids? Is IV rehydration better than oral? What is the evidence? Click here.

Dr Bishop gives you a brief summary of what the best available evidence says for a range of common clinical problems. No need to read all the articles and struggle with the data. Just get to the bottom line.


Use of Steroids in Tonsilitis

Are steroids helpful in the management of acute tonsillitis? Is a single dose enough? What about paediatric patients? Click here.

Dr Bishop gives you a brief summary of what the best available evidence says for a range of common clinical problems. No need to read all the articles and struggle with the data. Just get to the bottom line.

Diagnosing Appendicitis

Yes, appendicitis is a clinical diagnosis, then why does the surgical registrar asks for white cell count? When would you do an Ultrasound or CT for suspected appendicitis? What is the evidence behind these investigations? Click here.

Dr Bishop gives you a brief summary of what the best available evidence says for a range of common clinical problems. No need to read all the articles and struggle with the data. Just get to the bottom line.

Acute Atrial Fibrillation

Acute AF – Would you control the rate or go for rhythm conversion? What is your drug of choice? Would you anti coagulate these patients? What is the evidence behind your practice? Listen to this quick summary after an extensive research analysis. Click here.

Dr Bishop gives you a brief summary of what the best available evidence says for a range of common clinical problems. No need to read all the articles and struggle with the data. Just get to the bottom line.

Effective teacher in ED

[box]Bandiera (2005)

What do we have to do to be more effective teachers in the chaotic world of the ED?  A well conducted qualitative study from Canada.

The points that caught my eye were:

  1. The most commonly identified strategy was “Tailor teaching to the learner”; find out (very briefly) what they want to achieve this shift, this week, this term … whatever!! Know your trainees.
  2. Next was “Optimize teacher-learner interaction”; encourage the trainees to work through the problem for themselves and use “teaching scripts” (I liken these to the “Five Minute Talks” in Teaching on the Run).
  3. “Actively involve the learner”; challenge them to make a commitment, get them to make the decisions.
  4. “Agree on expectations”; tell seniors they’ll be expected to give a complete diagnostic and management plan so they know your expectations “otherwise they are all over the shop.”
  5. And then a whole run of the usuals; actively seek opportunities to teach, demonstrate a good attitude, be a role model, use additional teaching resources and improve the learning environment.
  6. Imporantly “provide and encourage feedback”. Timely, constructive, objective, impersonal, given in private, based on first hadn experience and a balance of positive and negative. Solicit feedback on your own performance – otherwise you won’t improve as a teacher!!  See the appendix for “Out-takes”; quotable tips and points!
Bill Croker

Intralipid for Calcium Channel Blocker Overdose

Read this interesting article; its just a case report not a recommendation.

Lipid Rescue of Massive Verapamil Overdose. A Case Report.

Conrad W Liang1, Sarah J Diamond2 and Daniel S Hagg2* 

1Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon, 97201, USA. 2Department of Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon, 97201 USA. Posted: 10/12/2011; J Med Case Reports. 2011;5(399)

Read Abstract [expand title=”Open” swaptitle=”Close”] Introduction: Massive intentional verapamil overdose is a toxic ingestion which can cause multiorgan system failure and has no currently known antidote.
Case Presentation: The patient is a 41-year-old Caucasian woman who ingested 19.2 g of sustained release verapamil in a suicide attempt. Our patient became hypotensive requiring three high-dose vasopressors to maintain arterial pressure. She also developed acute respiratory failure, bradycardic ventricular rhythm necessitating continuous transvenous pacing, and anuric renal failure. Our patient was treated with intravenous calcium, bicarbonate, hyperinsulinemic euglycemic therapy and continuous venovenous hemodialysis without success. On the fourth day after hospital admission continuous intravenous lipid therapy was initiated. Within three hours of beginning lipid therapy, our patient’s vasopressor requirement decreased by half. Within 24 hours, she was on minimal vasopressor support and regained an underlying junctional rhythm. After three days of lipid infusion, she no longer required inotropic agents to maintain blood pressure or pacing to maintain stable hemodynamics.
Conclusions: Intravenous fat emulsion therapy may be an effective antidote for massive verapamil toxicity. [/expand]

Amylase and Lipase

Dr Bishop gives you a brief summary of what the best available evidence says for a range of common clinical problems. No need to read all the articles and struggle with the data. Just get to the bottom line.

How good is amylase and lipase in diagnosing pancreatitis? Would you test for both? Which is better? Click Here












New Paediatric Stroke Scale Validated

The objective of this study was to evaluate IRR (Inter rater reliability) of a pediatric modification of the NIHSS, the Pediatric NIHSS (PedNIHSS). This is a MCT conducted at 15 sites in the United States and Canada from January 2007 through October 2009. Reported to have excellent IRR among child neurologists.

Abstract of the study,
[expand title=”Open” swaptitle=”Close”] Interrater Reliability of the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) in a Multicenter Study. Rebecca N. Ichord, MD et al.

Background and Purpose—Stroke is an important cause of death and disability among children. Clinical trials for childhood stroke require a valid and reliable acute clinical stroke scale. We evaluated interrater reliability (IRR) of a pediatric adaptation of the National Institutes of Health Stroke Scale.

Methods—The pediatric adaptation of the National Institutes of Health Stroke Scale was developed by pediatric and adult stroke experts by modifying each item of the adult National Institutes of Health Stroke Scale for children, retaining all examination items and scoring ranges of the National Institutes of Health Stroke Scale. Children 2 to 18 years of age with acute arterial ischemic stroke were enrolled in a prospective cohort study from 15 North American sites from January 2007 to October 2009. Examiners were child neurologists certified in the adult National Institutes of Health Stroke Scale. Each subject was examined daily for 7 days or until discharge. A subset of patients at 3 sites was scored simultaneously and independently by 2 study neurologists.

Results—IRR testing was performed in 25 of 113 a median of 3 days (interquartile range, 2 to 4 days) after symptom onset. Patient demographics, total initial pediatric adaptation of the National Institutes of Health Stroke Scale scores, risk factors, and infarct characteristics in the IRR subset were similar to the non-IRR subset. The 2 raters’ total scores were identical in 60% and within 1 point in 84%. IRR was excellent as measured by concordance correlation coefficient of 0.97 (95% CI, 0.94 to 0.99); intraclass correlation coefficient of 0.99 (95% CI, 0.97 to 0.99); precision measured by Pearson  of 0.97; and accuracy measured by the bias correction factor of 1.0.

Conclusions—There was excellent IRR of the pediatric adaptation of the National Institutes of Health Stroke Scale in a multicenter prospective cohort performed by trained child neurologists. (Stroke. 2011;42:613-617.)[/expand] Download Full Article in PDF,
[expand title=”Open” swaptitle=”Close”] PedNIHSS

Digoxin in AF

[S3_embed_video file=”Digoxin in AF.m4v”]

Quiz 2

Take the quiz

[mtouchquiz 8]

Article 1; Sep 2011

Acute Adrenal Insufficiency





EMA Courses 2012

EMA courses schedule for the year 2012 has been published and early bird registration available. Click here. For more conferences and handy TESL documents check the “Education” menu.



CT head Quiz

its obvious…

[wpsqt name=”CT head quiz” type=”quiz”]

1,2,3… It worked for me!!! May be for you too.

Wondering how to read and remember the basic sciences for the primary examination??? I had  the same thoughts; but  I worked it out.  When I prepared for my primary examination, I used a simple 3 steps rule; its a structured, focused method to cover the topics. So … my suggestion is …

  • 1. Read the chapter in the text book – with or without additional note making or writing in the book.
  • 2. Then go through the MCQs that pertain to that chapter. Demweb website is best as it has all the question organised by topic.Going through the MCQs and understanding the reason each is right or wrong directs you to all the details that the ACEM wants you to know.
  • 3. Next reading through the past vivas from the ACEM website completes each topic.


The Life in the Fast Lane website has images of the anatomical models used in the vivas.
Also for anatomy, it is easier with some physical bones to use but these are hard to come by.

This is how I found it best to study. It worked for me; maybe it’ll work for you too.

Good Luck.

Cindy Hastings

Formulating Clinical Questions and Literature Searching

[box]This is a quick guide to searching for evidence for clinical questions which you may encounter.

For example you may be wondering whether diazepam is effective in the treatment of back pain.

The clinical question should be structured in the PICO format :

  Patient population or clinical problem  =   back pain

   Intervention(study factor/exposure)  = diazepam

C  Comparator (control ) =   placebo

O  Outcome factor           =   pain

Your search terms would be the bold terms, although you could add other search terms if you were comparing other interventions eg. Paracetamol/codeine etc.

Databases and methods

All the following databases available through CIAP :

1) Cochrane database (under evidence-based practice tab in CIAP)– for systematic reviews

a) on the opening page, click the tab Advanced search

b) enter search term back pain

c) enter search term diazepam

d) combine with AND

e) under restrict search by product – tick ‘systematic reviews’ limit


2) Medline database – usually choose 1948-present

a)click on Advanced  Search tab

b) enter back pain – will be mapped to Medical Subject Heading(MeSH) term

c)Tick explode box to widen search, then continue

d) do not choose any subheadings, click continue

e) enter 2nd search term diazepam

f) click explode, continue, on the next page click continue

g)combine searches 1+2 by ticking boxes next to them and clicking AND

h) click on limits, then additional limits and select evidence based medicine reviews

i) click on search

Useful articles and links

Haynes RB, Wilczynski NL. Optimal search strategies for retrieving scientifically strong studies of diagnosis from Medline : analytical survey. BMJ 2004 : 328 (7447) : 1040

Haynes RB. McKibbon KA. Optimal search strategies for retrieving scientifically strong studies of treatment from Medline : analytical survey. BMJ 2005 : 330 (7501) : 1179[/box]

Worthy iPhone Apps

These are some of the iPhone apps worth to occupy few bytes among the Gigs of musics, videos and pics….

In no particular order,

1. iMIMS – Now available for free. Its available via ciap. But there are few steps to install it in your mobile.

Step 1. download the app from the apple’s app store and install it in  iPhone.

Step 2. login to Ciap from any hospital computer and register for MiMS on iphone through mobile resources. Once registered you will provided with a pass key/ code.

Step 3. Enter the code in your iphone and you are done!!!


2. Pedi Safe – great and invaluable app during those stressful moments in pediatric resusicitation. Select the weight of the kid and you have all the info you need to resuscitate the child; drugs, dosages, ETT size and more. American version, so beware of some drug units; otherwise its a life saver. Above all its for FREE.

3. Emergency Central

4. Eye Manual – Great app for those sitting in Fast Track. The eye atlas is a valuable resource for VAQ preparation. Just register in the app and its all free. ( Note – The NSW Eye Manual is still better than this. If you have a PDF reader (file app, documents to go, filesHD) you can upload the Manual and view it in iPhone.)

5. Documents To Go – Great app to synchronize your documents between iphone/ipod/ipad and your desktop (windows or mac). You have download the app from the app store and install it in iPhone. You also have to install an application at the desktop.  Once installed it will talk to each other and keep your files synchronized, You can edit your word, excel, powerpoint files either in iPhone or in your computer and just a press of a button, its synchronized and updated at all devices linked. If you want a keep a log of the procedures or cases in excel format, this is the way to go. You have to pay for this service ~$10, but money worth spending.

6. File App – Free app to move files from desktop to iPhone. You can move and open/view most of the MS office file formats but cannot edit your files in iPhone.

Ultrasound. Where do I start?

Focused bedside ultrasound examinations performed by trained Emergency Physicians in order to answer specific clinical questions, have been shown to improve patient outcomes. ACEM specifically supports the use of ultrasound imaging by emergency physicians for at least the following clinical indications: traumatic hemoperitoneum; abdominal aortic aneurysm; pericardial fluid; ectopic pregnancy, vascular access, therapeutic diagnostic tests and evaluation of renal and biliary tract disease. To read more about ACEM Policy, Click here.

So where are we? What are the options available to get trained and accredited?

Accreditation Body – Who has the authority to accredit you? Currently it is unresolved. ASUM offers DDU and CCPU courses which are kind of gold standard for getting accredited in ultrasound. Recently NSW health has come up with  a new accreditation process as part of the NSW health redesign programme with almost similar process involved in obtaining CCPU. Who is going to gain supremacy?  We have to wait and see.

Courses – There are million courses available to do and the number keeps increasing everyday. There is a course running almost everyday somewhere in Australia. But which is the right one for us? For a start look at the list of accredited courses for CCPU in ASUM website. It really doesn’t matter which one you do, as almost all of them has standard teaching schedule and will provide enough hands on experience. Start from a basic course and move forwards. Upon completion of the course, you have to practice at our workplace and maintain a logbook. DDU course has Part 1 and Part 2 examinations. Part 1 (MCQ) examination can be taken at anytime of your training but to sit for Part 2 examination, you should hold a Fellowship degree. More details about DDU is available in ASUM website.

We recently conducted a one day course in our hospital (thanks to Dr Stapleton, Dr Haig and Ms Hawkins) as part of NSW health redesign programme. Those who have completed the course are busy completing their logbooks. For further courses in our hospital, please keep checking our site.

Nepean ICU runs an ECHO Workshop called RACE and RACEplus, which is of invaluable asset in assessment of patients with chest pain, SOB and in CPR. More information is available in NICCER site.

To get trained in pelvic and first trimester ultrasound, Prof Condous is happy to accommodate one or two of us at AGS Clinic. Please contact Dr Stapleton if you are interested.

Its never too late to start your training in ultrasound. Just take the initial step and soon you will start to enjoy the magic of ultrasound waves. Happy Scanning.



Teaching on the Run

Teaching on the Run

Dr Fiona Lake and her team at the Education Centre, University of Western Australia  have produced an amazing program to help you become a better educator and clinical supervisor. The success of this program comes from its ability to be run in small groups, at your location, with the help of an experienced facilitator. Participate, facilitate and become a champion of this program in our local setting and see the improvement in how our junior doctors are supported during their training.

What does a Teaching on the Run workshop look like?

Six modules have been developed for the program:

1. Clinical (Bedside) Teaching
2. Skills
3. Feedback and Assessment
4. Supporting Trainees
5. Planning Term Learning
6. Effective Group Teaching

Each module runs for 3-4 hours, every week or when ever feasible. Participants should complete modules 1-3 before attending modules 4-6. The target audience is clinicians who have experience teaching undergraduate and postgraduate doctors, but who have had little or no formal teaching instruction.

Our emergency department is pleased to support this programme and everyone is welcome to participate.

More info, contact

Dr Bill Croker

Emergency Department



Ambulance Bay