Category: clinical

Emergency Services Show 2012

I will be at the Emergency Services Show 2012, held this week Wednesday and Thursday (21st and 22nd of November). Looking forward to meeting new people, catching up on the latest technological developments and getting some CPD from the College of Paramedics.

There will be a couple of us meeting up on Wednesday at 1215hrs outside the College of Paramedics stand (Hall 3, stand E71, floorplan here). I’ll be live-tweeting together with a bunch of fellow tweeters – be sure to follow the #ESS2012 hashtag.

Hope to see you there!

GTN as a diagnostic tool

Last year, I posted about a presentation at the Paramedics Australasia Conference:

[click on picture to download full PDF]

According to the authors reviewing the literature, GTN is rubbish as a diagnostic tool.

I received some comments (on- and offline) of astounded people about this. I followed up with the authors, but forgot to post the reply. Many apologies.

A big thanks to the authors, Lynsey Smit and Laura Roberts (both from Monash University), for allowing me to post their presentation online. They can be contacted via email address: larob7 [at] & lsmi19 [at]

Ketamine Firetruck

Feuerwehr Taufkirchen Source:


A recent thought provoking comment was posted on twitter by spanish doctor Alexander Sammel (@socalexmed):

Well…we can’t leave that uncommented, can we?

Ketamine seems to be seriously coming in to ‘fashion’ amongst healthcare professionals in emergency settings, and advocates for a variety of uses are popping up everywhere you look. Applications include pain management (interesting discussion) and (procedural) sedation, Rapid Sequence Induction (RSI) and possibly depression.

But coming back to the initial statement. “Prehospital medicine without Ketamine is like a firetruck without water!!!”

Not every firetruck needs to carry water. Not every paramedic needs to carry Ketamine. For bushfires in rural and regional areas, it would be prudent for the fire brigade to carry water to the fire in order for it to be able to extinguish the flames. In more built up areas, there are hydrants available. And some fires can’t be extinguished by water – foam is needed.

Similarly for paramedic practice, Ketamine can be a great drug in the right hands; for those with the right training, experience, and exposure. This is most likely to be a Intensive/Critical Care Paramedic. The majority of patients don’t need Ketamine, but for those that do, you want a Paramedic in the know. For other jobs without the need for Ketamine, Paramedics that aren’t carrying Ketamine can respond. And if Ketamine is needed – they can be backed up by a Keta-medic.

Personally, I have used Ketamine multiple times for patients in severe traumatic pain, and it has worked a treat. Sometimes, Fentanyl (or Morphine) just doesn’t do it (e.g. severe burns or long bone fractures).

So – in a way, Paramedics without Ketamine are like fire trucks without water. They come in all shapes and sizes, and each ‘model’ has their specialty.

The conversation on twitter can be viewed here: Thanks to Matthew Harris (@HarrisCPD) for sharing the initial tweet.

Nebulised Naloxone

A recent blog post by Dr. Cliff Reid (@cliffreid) alerted me to a study done in the USA on nebulised naloxone.

An interesting concept, and laudable that needle-less approaches for these tricky patients (dodgy veins, high risk of blood borne disease) are being trialled – I have written on intranasal application of medication previously.

I had a read of the paper accessed via my uni library (so that’s where all the tuition fees end up), seemed decent enough on first glance.

Two questions did arise though:

  1. In my experience, for a nebuliser to work, the mask (and therefore the patient) needs to be upright. Most patients who would require ‘naloxonisation’ would present lying down. I am not a fan of wrestling patients, deadweight or not. Is there a way of administering a nebule whilst the patient is in a horizontal position?
  2. Opiates/opioids have the effect of decreased respiration – both rate and depth. I’m sure this would have an effect on the uptake of the medication. It may be a good addition to include a T-piece, which would enable ventilatory support via a Bag-Valve Mask, thus increasing respiration depth and rate, and amount of naloxone administered.
What do you think? Do you have experience with any of the above? Leave a comment, tweet me or email me!
I have written an email to the authors of the paper…stay tuned for any responses.

Act F.A.S.T.

I came across an interesting fact recently, a fact worth sharing:

In an ischaemic stroke, cell death occurs at a rate of 1.9 million neurons an hour. This is the equivalent of the patient ageing 3.1 weeks every minute (1)

Makes you reconsider what is actually going on in the brain. For successful treatment and a (near) full recovery, time is of the essence…as the best anti-ageing potion.

There is a definitive time bracket for the treatment of ischaemic strokes with tPA (Tissue Plasminogen Activator) – where I live the cut of time is 4.5 hours from symptom onset (2)

Many stroke symptoms are recognise too late – remember, time is brain, and the public need to be aware of common stroke symptoms. The F.A.S.T. mnemonic has been an initiative by the stroke foundation here in Australia:

But we as Paramedics can also have a positive impact on suspected stroke victims – by recognising the signs, transporting the patient to an appropriate facility and pre-notifying the staff of our arrival (3).


What are your stroke guidelines and procedures?



1 Saver, J. Time is Brain – Quantified Stroke 2006;37:263-6 via Michael Moldoveanu “Delays in Thrombolysis for Ischaemic Stroke Patient: Implications for Paramedic Care” Response Spring 2011 (Volume 38 No. 3), Paramedics Australasia.

2 p.27, Model of Stroke Care 2012, WA Dept. of Health.

3 p.24 Model of Stroke Care 2012, WA Dept. of Health.

Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain;jsessionid=B56BA8474F1D8E28F05588AFC5CF3837.d01t01

Neurons, Synapses, Action Potentials, and Neurotransmission



If you are wondering how many neurons the human brain is actually made up of, estimates range from approximate 86 billion (4) to 200 billion (5). So in terms of percentage of neurons actually dying an hour, this equates to roughly 0.0000221% to 0.0000095%. Which would translate in to waiting approximately 45 249 to 105 263 hours (1885 days or over 5 years to 4385 days or over 12 years) for one percent of the brain to have died. Multiplied by 3.1 weeks a minute…oh sod off, I can’t be bothered. Do it yourself 🙂





RINSE and repeat.

The service I work in has very recently began collaboration in a pretty cool (pun intended) trial – the RINSE Trial (Rapid Infusion of Normal cold SalinE).

Why: Current guidelines only support the use of therapeutic hypothermia post ROSC (Return Of Spontaneous Circulation) – see the Australian Resuscitation Council (ARC) guidelines or the International Liaison Committee On Resuscitation (ILCOR) advisory statement. The RINSE trial was initiated to find out if there is any clinical benefit in commencing therapeutic hypothermia during resuscitation efforts by paramedics.

Background: Basically Therapeutic Hypothermia (TH) aims to slow the rate of metabolism down, reducing the body’s consumption of O2, and also lessening the chemical reactions that lead to reperfusion injury (reference). For a even more info on TH, visit the ever excellent Life In The Fast Lane and EMCrit.

How: Paramedics will be inducing TH by means of IV chilled Normal Saline, checking temperature via tympanic thermometers.

Who: This study is currently running in three states in Australia, by the three statewide Ambulance Services and a participating university in each of those states:


Please check out the link for more and in-depth information!

RINSE trial


Has your service implemented TH for cardiac arrest?

Atropine induced hyperthermia

A good friend recently asked me whilst studying: “Atropine can cause hyperthermia – why?”

He had only learnt this a few hours prior, and I had heard this for the first time at all. I am not very familiar with atropine – we don’t use it in our service. All I really knew until then that it is a parasympatholytic – and purely based on that word, it became my favourite drug. Parasympatholytic. Para-sympatho-lytic. What an excellent word. Mmmh. Medical Terminology Porn.

Anyway…enough drooling.

This article came up in a quick search, and put me on the right track. Read it for an in depth look; here is my simple version:

Atropine antagonises central muscarinic receptors (remember, the parasympathetic nervous system is made up of muscarinic and nicotinic receptors). This muscarinic receptor antagonising alters temperature regulation in the hypothalamus – the mechanism how it works is unfortunately not understood. But is is known that it reduces blood flow to the skin, thus reducing the ability for the body to lose heat and increasing body temperature. Similar to Adrenaline (Epinephrine for you North American types) I take it, although a brief search could not link adrenaline to hyperthermia (if you know of anything, please let me know).

And as a nice bit of side information the article describes the difference between fever and hyperthermia. So, go on, have a read!

Mechanisms, management and measurement in atropine induced hyperthermia (Anaesthesia and Intensive Care, March, 2009 by K. Gillman)

Intranasal Medication Administration

The intranasal route of medications seems to be growing in application. This article by Kane (@antidoped) from LITFL brought my attention to a whole new array of intranasal (IN) applications. I was aware of trialling IN Naloxone (e.g. here, and a list of trials here); and the service I work in uses Intranasal Fentanyl for pain relief.

IN Fentanyl has produced satisfactory results in most cases to my liking. The main positive aspect to mention is the quick, easy and pain free application (extremely beneficial for already anxious patients, those with needle phobias, and paediatric patients). The down side list is a little longer though: Many people in pain cry, or in some other way get a snotty and blocked up nose – deeming this route ineffective. I have had some people reporting up to 7/10 pain, and still refusing a squirt of liquid up their nose (questionable reasons, I won’t go in to more details). Application is not always straight forward, some people excessively (against all carefully formulated instructions and advice) breathe in or out during administration, reducing the effective dose. Sometimes seemingly half the dose still runs out of patients noses, or runs down their throat and is swallowed. Discrepancies between given and absorbed doses are bound to happen.

The obvious that IN application brings with it is that it negates the need of IV access, or an IM needle, thus reducing the potential for needle stick injuries. Great for dodgy situations e.g. administering naloxone to a potentially HIV and Hepatitis ridden junkie, or getting some anticonvulsant in to someone actively seizing. Hypoglycaemia, a favourite patient to stay at home (under appropriate circumstances of course), too.

But it shouldn’t be the only option. As stated above, not all patients (especially in the out of hospital environment) have patent nasal passageways, and anyway…if you’re administering powerful medications to patients, you would want a line up just in case.

Or would you? That is a topic for an entirely new post. At the end of the day I recommend looking at the use of intranasal administration of certain medications. If you already are using this route, why not see if you can expand the range of meds given? There are many benefits, most of which relate to the first two rules of a paramedic: #1:crew safety, and #2:patient comfort and wellbeing. Read up the whole story on, and I would be pleased to read any experiences you may have with IN medications in the comments section below. And if you do get your hands on an atomizer, I suggest to squirt some normal saline up your own nose, in order to know what you are putting your patient through.