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Electrical Injury - who needs to be monitored?

Tuesday, July 6th, 2010

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Electrical injury, although not a common occurence can present with significant injury. Often the extent of the injury can be under-estimated as it mostly occurs below the skin, with little more than an entry and exit wound to see.
The very fact that patients with these injuries don’t present often, can result in management challenges. These can range from resuscitation approaches, to decision making as to who needs to be monitored.

The obvious high voltage exposure, with significant burn and injury, is not really a challenge in terms of monitor/non-monitor decision making. The challenge is from that group of patients that are well, with minimal injuries. Who, if any, of these patients do we monitor?

Electrical burns have a trimodal distribution:
1. The first peak is in children. This is primarily due to behaviors such as cord biting.
2. The second peak is in adolescents who engage in risky behaviour and the third group is:
3. Those whose work involves electricity and potential exposure.

Childhood injuries are usually biting injuries, where the child will chew through an electric cord. The result will be a burn to the lips or mouth. These burns are usually bloodless and painless as the vessels have been cauterised and the nerves damaged. One of the main issues in dealing with this kind of elelctrical injury is how to approach the burn itself. These burns will result in significant contractures and current management strategies, which are controversial,  include plastics repair and/or mouth splints.
The two main questions with children are:
Do we admit all these children? and
Do we monitor them?
At one time all children were admitted, however more and more, unless there are social or other issues, children with circumoral burns can be discharged. The one thing that may occur in about 10-15%, is delayed bleeding of the labial artery. This occurs some ten days following the injury. The only treatment needed, if the child is at home and bleeding commences, is pressure over the area and representation to the emergency department.

Can we send these children home from a cardiac point of view, or do they need to be monitored?
Bailey et al (Ann Emerg Med 1995;25(5):612-17) looked at household injuries involving 120V and 240V and concluded that no ECG or monitoring was needed. This study had some limitations in that it was retrospective and didn’t look at those potential higher risk groups with loss of consciousness, tetany and passage of current through the heart.

In 2000 Bailey revisited the higher risk group(Am J Emerg Med;2000 Oct:18(16)621-5) and performed a prospective study evaluating guidelines for monitoring high risk patients. 224 children were included in this study and the criteria for 24 hours of monitoring that were tested were:
1. past cardiac history
2. loss of consciousness
3. voltage greater than 240V
4. Abnormal ECG
There was no mortality or morbidity.
Bailey has gone on to do further studies which we will discuss shortly. In children therefore there is very little reason to monitor. If you still feel uncomfortable with no monitoring, then I would still monitor the following:
1. loss of consciousness
2. past cardiac history
3. high voltage

The next group to consider is adults without a severe injury, that we are considering monitoring.

Fatovich(MJA 1991 Sept 2;155(5) 301-3) looked at who needed monitoring following household electrical injury at 240v and 50Hz. This was a small study with 50 patients, however the conclusion was clear. No monitoring was needed in patients who were asymptomatic with a normal ECG.

Bailey (Emerg Med Journ 2007 May;24(5):348-52) conducted a prospective multicentre study involving 21 emergency departments. 143 patients were enrolled with what were considered, significant factors. They were:
-transthoracic current
-tetany
-loss of consciousness
-voltage>1000V

No patient in this study developed lethal arrhythmias. The conclusion was that patients with low voltage injuries with no loss of consciousness and a normal ECG, did not need monitoring.

So lets make some sense of all of this.

In children, most low voltage injuries do not require monitoring. The exceptions would be those children with cardiac history.

In all patients with minor injuries who are asymptomatic, have been exposed to a low voltage(<240V) and have a normal ECG, monitoring is probably not required.

Peter Kas

Posted in Cardiology, Resuscitation, Trauma | 2 Comments »

ventricular tachycardia and methadone

Sunday, June 20th, 2010

A 42 year old male with a past history of IVDU and alcohol abuse and brain injury, presents with what looks like withdrawal. Current medications included methadone and earlier on the same day, he was commenced on naltraxone.

Initially he is found to be becoming progressively more agitated and having brief episodes of depressed conscious state, with improvement between. He is ‘jittery’ with myoclonic movements in the bed. On vitals, he is found to be afebrile with a fluctuating Glascow Coma Score, bradycardic, and to have a systolic blood pressure of 80mmHg, and so he is taken to a resuscitation cubicle.

Is he in withdrawal?
Is he seizing?

As I enter the resus cubicle to find out why the patient is there, I notice a wide complex tachycardia at a rate of about 230bpm. He is still moving. It is self limited after a few seconds. Then a further episode.

In between episodes we do this ECG:
img_05523

It shows a bradycardia at rate 42bpm, there are tall T waves and premature ventricular complexes. There is a hint of a sinusoidal wave form in V2-V3(but no bundle branch, so not Brugada).
Is it ischaemia?
The QTcorrected. It’s 524ms. A QT corrected of greater than 450ms is considered prolonged.

The diagnosis is; prolonged QT causing Torsades.

Here is the next ECG we take as he begins an episode.
img_0553

So now we see a bizarre wide complex tachycardia, that looks like Torsades, with very abnormal QRS complexes following and the telltale signs of of patient shaking and agitation.
It is self limiting.

We commence Magnesium infusion in this patient. His K is 3.5, so we increase that also.

He then has a further episode which is on the rhythm strip below:
img_0555

He needs cardioversion for this.
He is intubated and soon stabilises. We do one more thing and that is, get a head CT. Why do we do this? There are a small number of cases where increased intracranial pressure can cause prolonged QT. Given his history of IVDU and alcohol, we want to exclude a subdural, or other lesion.

It is normal.

Cardiology review prior to stabilisation and want isoprenaline to increase the heart rate.
Why do they want this? ………..Read on.

Let’s look at QT prolongation.

It is caused by:
-hypomagnesemia
-hypokalaemia
-hypocalcaemia
-Na channel blocking drugs, such as Type I drugs
-raised intracranial pressure
-acute coronary syndrome
-hypothermia
-hereditary causes such as Lange-Nielsen(QT and deafness) and Romano-Ward(no deafness)

Management is Magnesium and in more severe cases of recurrent Torsades an implated defibrilator.

WHAT CAUSED THE QT PROLONGATION IN THIS PATIENT?

Most probably Methadone.
It is a synthetic opioid that is metabolised by the cytochrome P450 pathway and affects Potassium ion channels.
Studies have found that it causes significant increases in the QT interval (Martell et al, Am J Cardiol 2005;95:915-918)(Krantz et al, Pharmacotherapy 2005;25:1523-1529), especially in those on a maintenance dose greater than 40mg/day.

Why was isoprenaline recommended by cardiology? Quite clever really…
We know that Torsades is caused by QT prolongation, so increasing the heart rate decreases the QT as per the following formula:
QT = 656/[1+(heart rate/100)] (Ravtaharjus’s formula)

The patient stabilised on Magnesium and Potassium, without isoprenaline and he went to an ICU bed, with a plan to manage and substitute his Methadone.

So beware the IVDU patient on methadone that presents with syncope. We often put the symptom down to the patient having used heroin or a similar drug. Do an ECG and look for a prolonged QT, although uncommon, it may have been an episode of Torsades de Pointes.

Peter Kas

Posted in Cardiology, Case Studies, Resuscitation | Comments Off

Could this be a Pulmonary Embolism?

Tuesday, June 8th, 2010

In a previous blog we looked at the following patient who presented to the emergency department:

62 year old male presents to the Emergency Department with what he calls a flare-up of his congestive cardiac failure.

He states he is short of breath. He is a frequent presenter to the department with this complaint. He has not taken his frusemide for the past 48hours. He states that he feels very tired.

He is a well looking man with normal vitals Heart sounds dual, no murmur. normal JVP, bilateral pitting oedema to mid calves. Chest clear Abdomen soft His ECG and CXR are normal Bloods including a troponin are normal.

I’m unsure of the diagnosis, but given he hasn’t taken his frusemide, I treat him with that. I am going to discharge him, however it is late at night and he lives alone, so we decide to keep him in the department overnight. In the morning, he looks well and feels better, but still lethargic, ECG is unchanged, but for some reason someone does a follow-up troponin and it is 4.

He is diagnosed with a NSTEMI and sent to cardiology.

I now ask the question could it have been a pulmonary embolism and not a NSTEMI?

Certainly if we look at this case we see that the patient had dyspnoea with a normal chest on auscultation and on chest X-ray. Hmmm…

What are the risk factors for pulmonary embolism? Well we know of the classic ones of anything affecting Virchow’s triad. There are the hereditary factors of Protein C and S deficiency as well as others and the acquired factors such as immobility, recent surgery, cancer and others.

This patient had congestive cardiac failure(CCF). Is that a risk factor? As it turns out it is. In a population based study by Helt et al (Arch Intern med. 2002;162:1245-1248), the attributable risk associated with venous thromboembolism was 9.5%. So there is an increased risk in CCF.

What about symptoms and signs? Surely they would help.

Stein et al (Chest 1991;100:598-603), looked at patients with a suspected pulmonary embolism(PE) and with no previous evidence of cardiac or respiratory disease.

He then looked at the symptoms in patients with PE(n=117) and those without PE(n=248) as follows:

Dyspnoea - 73% with PE had it, but 72% of those with no PE also had dyspnoea.

Pleuritic Pain - 66% with a PE had it, and 59% without a PE also had it.

Leg Swelling - 28% with PE had it and 22% without PE had it

None statistically significant.

Well how about signs, surely they must help?

Tachypnoea - 70% with PE had it as did 68% of those without PE

Tachycardia - 30% with PE had it as did 24% of those without PE

Deep venous Thrombosis- 11% had it in both groups

Nothing was statistically significant.

What is interesting is that 97% of patients with a PE had

DYSPNOEA

or

TACHYPNOEA

or

PLEURITIC CHEST PAIN

So be on the lookout for those.

How about the TROPONIN rise- surely a pulmonary embolism can’t cause that?

Well as it turns out it can. Although we are unsure of the pathophysiology, it is postulated that it is due to increase in right ventricular afterload and irreversible ischaemia. It is also a predictor of in-hospital death (Giannitsis et al Circulation;2000;102:211-217). It’s important to say that the troponin rose in a group of patients that had suffered at least a moderate if not a large PE.

Those with a small PE may not have a troponin rise.

So the level of troponin rise is important as a rise of >0.1 is a potential predictor of mortality, however in the above study, none of the troponins rose above 1.0.

One other important characteristic was that the troponins rose earlier, ie., within 3-5 hours, in PE.

Therefore it is important to note that although troponin can rise, it usually does not do so, to as high a level as when true cardiac ischaemia occurs.

So, how about my 62 year old gentleman - could it have been a PE? The answer is yes it could. What is against it, is the level of rise of troponin was probably too high for someone looking so well.

Could it have been a thoracic dissection?

We’ll look at that next time…….

Posted in Cardiology, Fellowship Exam, Respiratory, Resuscitation | No Comments »

I’ve changed the way I do surgical airway

Saturday, April 24th, 2010

I think there’s a better way. This comes after talking to people who’ve done ton’s of surgical airway. When you work in Australia and don’t get the volume of patients that have the trauma and other conditions that will lead more often to the surgical airway, you define your technique to suit what you do and this is what we’ve done in the past.

But now we ask, is there even a better way?

What better way to learn than to ask Emergency Physicians in the country where surgical airways are more common than corn chips - OK maybe that’s not quite true, but you know I’m talking about the US of A.

Many of you have attended my airway workshop. Given that its one of the only workshops of its kind in Australasia, where do I go if I want to see if I can get challenged? Yes sir, “I saddled up the truck and moved to Beverly”(most of you younger guys won’t know this quote, but the older and more arthritically challenged amongst you, like me, will know that line is from an old series,’The Beverley Hillbillies’.

Anyway, I was taking an airway workshop and talking to the guys from USC and we had a discussion on airway and especially surgical airway.

I showed them my horizontal technique and discussed the issues related to it.

Now let me put this in context for you, and a little bit of a rant will follow! This rant is about the way anaesthetics or ICU or anyone else reacts when the ED does a surgical airway. It should be supportive and create an environment for learning. It many cases, it creates a hostile environment. That saddens me.

A few years ago I was working at a trauma centre down South in the land of OZ and there was a case where one of the emergency physicians had to perform a surgical airway. The details aren’t important. What is important is that after this, the anaesthetics department were up in arms and even had MRI’s done on this patient, to prove that the airway was in the wrong place! Why?! Why is there this desire to prove the ED wrong?  The Emergency Airway is our domain and we should deal with it. What we should have is the understanding and support of colleagues.

Anyway, after all the MRI’s, the tube was in the right place, in the cricothyroid membrane. The patient went home two weeks later.

In this same department, our anaesthetics colleagues were then trying to stop the ED from using propofol - what’s going on here?

More recently, I heard in another ED, that  there was another issue related to surgical airway, where there was a complaint made about a surgical airway being done by the ED consultant and again all the doodoo hit the fan. Again, all was done correctly with tube in the right place.

When I recounted these stories to our US colleagues they were a little taken aback. The emergent airway is the domain of the ED. Full STOP, Period, END OF STORY!

So, hopefully as we all do these airway and procedures workshops and improve our skills, the hostile approach will give way to mutual understanding. Now I’m not saying that all anaesthetists are like that. Its just that some circumstances bring out strange behaviour.

My thoughts on all of this was, how can we even make it better? How can we minimise the chances of missing? If we get better at what we do, and believe me when I say, that knowledge is power, then these ‘misunderstandings’ will occur less and less.

As most of you who have done the airway workshop know, I favour locating the cricothyroid membrane)( and we go into the anatomy of this) and then:

-make a horizontal cut

-put something in the hole, either suture, holders, or a clamp(someone recently recommended, a bougie)

-remove the scalpel

-then feed the size 6 tube, or a small ’shiley’ trachy over this.

BUT the thing I’ve noticed is that the big issue that others have is; ‘are you at the right level?’ Have we in fact not cut at the level of the cricothyroid membrane and cut at some other level and then what do you do? You either don’t realise it and put the tube in where you are, or you have to make another cut! This is a real issue, so how can we make sure we remove this type of error as best as possible?

THE NEW TECHNIQUE

Make a vertical cut - A GENEROUS VERTICAL CUT- this can be 5cm long. You need to get through all the skin with this.

Then with your finger feel down until you find the anatomy- this is where the pig’s trachea that we use in the workshops, comes into its own, as it feels like it.

Once you’ve found the cricothyroid membrane, then put a horizontal cut in it and then feed in your tube as per the method we already use.

That’s it! A simple change, but with a potentially massive result.

I’ll be showing this at the airway workshop - in May and in July at RESUS 2010.

Have fun, enjoy your work and remember that the knowledge you take into your shift DOES matter!

Peter Kas

Posted in Airway, Procedures, Resuscitation | No Comments »

Basic Life Support and Resuscitation

Wednesday, March 31st, 2010

This is a little video we did a while ago for the medical students and gives them a practical approach to an arrest scenario. Bad acting aside, it does the job.(As many should notice, the only thing we don’t do first is give the initial 2 breaths).
The video takes a few seconds to start.

Basic Life Support is a key skill for all of us. I mean for ALL of us. In Emergency medicine we resuscitate often and so we almost take it for granted that we know this material. If you are a General Practitioner, a healthcare practitioner of any sort, be it surgeon or physician, you need to know this. If you are a nurse, you need to know this. Those of you who are not medical practitioners, but may be dental practitioners or even that subgroup that undertakes sedation of patients, you need to know this!

In medicine, whether you see oncology patients every day, take out gallbladders, or provide family medicine, it is expected of all of us and we must expect it of ourselves, that we know this stuff backwards. We must know the basics of resuscitation.

Just when you were getting it, ILCOR will bring out something new this year. Odds are that the number of compressions to breaths will again increase, highlighting the importance of chest compression and maintenance of coronary perfusion pressure. In fact, I’ll stick my neck out and say that airway will take a minor role in BLS after the new guidelines come out. In fact in BLS, the only thing that makes any difference is chest compressions! In ACLS, and this is not the time to talk about it, the only things that make a difference are defibrillation and cooling. The only other thing that comes out of the latest literature is the benefit of hot coronary angios in patients that have arrested. But more on this in an upcoming issue.

There are two things to remember about arrests. Adults usually have cardiac arrests secondary to ventricular fibrillation or other non-perfusing rhythm. They infarct, have an arrhythmia and die. In these patients one of the most important things we can do is defibrillation. If you find them in the first 3-4 minutes, defibrillation is the key. If you find them after 4 minutes, doing a little CPR before defibrillation is important. This has to do with the ‘electrical’ and ‘circulatory’ phases of the heart. More about that on another blog.

In contrast, children usually have arrests secondary to respiratory causes. They usually have an airway issue, become hypoxic and then arrest. There are those of course that have congenital cardiac conditions, that may still have a cardiac cause of arrest, however, the predominant cause of arrest in children is respiratory. it is important to work on their breathing first. Open their airway, deliver some breaths, then CPR.

1 There is no real evidence on the best ratio of breathing to chest compressions. There is evidence that maintaining coronary perfusion pressure is advantageous and therefore a minimal interruption to chest compressions is very appropriate. I remember years ago, many a time, when we delayed compressions by searching for that pulse. We couldn’t find it in the wrist or the neck, so someone would check the femoral and they may not be sure, so someone else would then check it. …..The result would be several minutes of delay. Significant, knowing what we know about how quickly coronary perfusion pressure falls.

With this, the introduction of the new ILCOR guidelines this year are expected to yield even higher compression ratios. Remember that we have progressed from 15:2 to 30:2. It is plausible the the ratio of chest compressions to breaths may increase even further. Is there any evidence for say 50:2? There certainly is no evidence against it. We know that the aortic pressure(used as a surrogate marker for coronary pressures) drops significantly when cardiac compressions are stopped for breathing. This was for the old 15:2.
Watch this space, as I’m sure I’m right about this. So basically, push the chest hard, push it fast and push it deep, and keep pushing it.  Sometimes you will feel something crack- keep pushing. After defibrillation, start cardiac compressions right away, don’t stop and take the pulse. If the patient wakes up, they will let you know, believe me!  … and if I’m right, soon we’ll be told to push more and blow even less.

A little while ago the ‘Spark of Life Conference’ had some T-shirts for sale and they had an area in the centre of the chest that said “push here” and an arrow pointing up to the head and that read “blow here”. It’s really as simple as that.

2 Be careful with your ventilation. Over ventilating a patient is something we are all guilty of. if you are bagging a patient, then you need to be careful not to over-inflate the lungs. Certainly sometimes after we tube the patient, there is a tendency to try and make up for the few minutes we were not ventilating and we furiously pump the bag, getting that oxygen in. I’m guilty of this too.

There is very good evidence that in a resuscitation scenario, more than 10 breaths per minute is associated with ZERO return of spontaneous circulation(Circulation 2004:109;1960-65).

Who has heard of  the ‘Lazarus Phenomenon’ (if you’ve been to the Airway Workshop, you’ve heard me talk about this), where a patient we thought deceased, has got an output back? In these cases the cause is believed to be hyperinflation of the patient’s lungs, increased intrathoracic pressures, thus a decreasing venous return to the heart and a decreasing cardiac output. Stop the bagging, disconnect the tube and the lungs go down, cardiac return starts as does cardiac output and before you know it, BEEP, BEEP BEEP, is what you hear on the monitor.

Ventilation is not only about rate, but also about volume. If an adult bag holds 2500ml and we know that the tidal volume we need to give say an 80kg male is about 800ml or so, then why try to squeeze the ‘heebeegeebees’ out of the self-inflating bag. Try for about half the bag.

So ventilate at appropriate volumes and keep the rate at <10 breaths per minute. A greater rate of ventilation than this, in an arrest, has been associated with no return of spontaneous circulation. Circ 2004:109;1960-1965

3 The depth of compressions worries me. It is true to say and several studies have shown that the rate and depth of compressions suffers with time. Basically at less than about 2 minutes. What is more important is that we don’t recognise that our technique is suffering. It should really be a rule that the person who performs CPR should change over every 2 minutes, ie., every pulse check. This is so important and we may find that given the importance of chest compressions, this is an area that we must all be doing well.

A couple of other things to say. I am very excited about the use of ultrasound in arrests and we use them all the time, especially if we are unsure of cardiac activity. How advantageous it is to be able to see the myocardium and know if it is contracting or not. I invite you all to use the ultrasound machine if you are fighting with a resus and can’t get anywhere. Look at the heart  to see if there is cardiac motion. The best view really is not the subxiphoid view that we use as part of the FAST examination, but a parasternal view where we can easily visualise the left ventricle, mitral and aortic valves and the outflow tract. This is not that difficult to learn. More about this in the near future- some videos coming.

The question of when to stop is a difficult one and one that needs a significant discussion. That’s really for another blog. Basically if someone has been in asystole for about 9-10 minutes with no output, you can stop, unless they are hypothermic. These patients will not survive. In cases where you have been going at resuscitations for 25 - 30 minutes with no spontaneous return of circulation, again it is time to consider stopping.

What about children, that have been found unresponsive ie., SIDS, or children that have arrested in hospital. How long do you resuscitate there? What about if there are staff members that don’t wish to stop a resuscitation What then? This is a very difficult area and although there are some guidelines, you need to be comfortable with what you wish to do.

Basic Life Support is just that, basic. For those of us that do this regularly, it’s easy to become a little complacent. It’s easy to say, well the  evidence this and the evidence that. The reality is, that this is the best evidence we have and we must use it.

In terms of priority, considering the adult population, if you get to them with a defibrillator shockem, if they have a shockable rhythm. if not, chest compressions are the priority, push hard and ofter(trying doing 100/minute for two minutes and see how hard it is). If you can, some airway is good. Stick to the 30:2 for now. Change operators regularly. This is basic, but not easy. Good Luck.

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Advanced Airway Course at Albury Wodonga

Sunday, March 14th, 2010

Thanks to Alex Swain Director of Wodonga Emergency for inviting us up to Albury Wodonga to give an Advanced Airway Workshop. It was a great day and everyone played all out. It was a real treat to see the layered approach of teaching kick in and by the end of the day everyone could tube every manikin repeatedly…..even the famous manikin(dubbed this over several workshops) ‘Mr Evil’. This is even after I had changed all the anatomy ie., tongue up and larynx partly swollen and vocal cords slammed shut!

What was also great was the discovery, as we called it, of the ‘Swain technique’. Alex thought about surgical airway and his solution was to make the cut in the cricothyroid membrane and then put a bougie in there, and railroad the tube over it. I LIKE IT!

Thanks again everyone. Airway is not difficult. It’s essential and with the right teaching you can learn how to establish an airway every time!!! You don’t need the fancy gadgets. You don’t need the thousands of dollars of equipment if you cant afford it. All you need is:

-a curved blade laryngoscope(#3)

-a stylet in the endotracheal tube bent at 35 degrees ie ‘hockey stick’

-a bougie

If all else fails, then simple things  should be available, such as an intubating laryngeal mask or an ‘airtraq’ and have on standby  a 14# cannula and some tubing for jet insufflation or just a scalpel for the definitive surgical airway. Remember, the most difficult thing about the surgical airway, is the decision to perform the surgical airway. As I’ve shown you, the technique takes only 20 seconds.

REMEMBER TO HAVE A PLAN. When will you decide to go to the next step. The definition of a failed intubation is 3 failed attempts at passing a tube by an experienced operator, OR sats < 90%. Know when you must make the decision to go to surgical airway. The most important thing about intubating is position and putting the blade in the right place ie., the tip of the blade in the vallecula and  then pulling up in the direction of axis of the handle.

Make sure your basic techniques are sound. Practice those bag-valve-mask techniques as they may be what saves your patient in the end.

Well done guys and I look forward to catching up with the bunch that registered for RESUS 2010 at the conference in July.

Again thank you all for your committment to learning.

Peter Kas

DOWNLOAD THE ADVANCED AIRWAY PDF

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Central Line Placement with Ultrasound

Wednesday, January 20th, 2010

Central Lines can be very difficult to place. True central lines are the subclavian line and the internal jugular line. There is also the provision for insertion of a femoral.

Subclavian lines can be easier to establish as the subclavian vein is a permanently distended vessel that is relatively easy to cannulate. There can be contraindications, or situations that make the subclavian difficult. Apart from direct trauma to the area, one of the most common reasons for inserting an internal jugular, is potential coagulopathy. The IJ gives us the ability to apply compression forces, whereas the subclavian, which passes under the clavicle, is protected by bone and there is very little provision for direct compression to stop bleeding.

The use of ultrasound as shown in this video, allows us to clearly see the compressible vein and also us to see the point of insertion of the needle, in the vessel. This is a very safe technique and relatively simple to master. It has the benefit of allowing you to directly see entry into the vein, as well as minimising the incidence of pneumothoraces.

This will be one of many procedures that can be practiced at RESUS 2010. This is really shaping up to be a great conference, with attendees joining from all over the country. I look forward to seeing you there.

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RESUS 2010 Australia

Sunday, December 20th, 2009

Here is the shortened version of the movie for RESUSCITATION 2010 Australia. Everything on resuscitation over two big days.

This is two days in one of Melbourne’s most beautiful areas, overlooking Albert Park Lake. With this backdrop, we are putting on a two day spectacular. Big Speakers, Big Topics, Big Screens, Big Prizes and a multimedia feast!

Click on the sidebar to find out more!

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RESUS 2010

Wednesday, December 16th, 2009

RESUS 2010 is a two day conference totally dedicated to resuscitation. When I first started planning this conference nearly a year ago, it was obvious that there was nothing of this kind in Australia. I wanted to provide doctors, nurses and paramedics with something that they could attend within Australia and not have to travel overseas to get.

We have put together some of the most knowledgeable speakers, to talk on a range of topics from resuscitation guidelines to acute coronary syndrome, pulmonary embolism and arrhythmias, to trauma resuscitation and paediatric resuscitation and so much more. Our speakers include Dr John Katsoulis, Head of Internal Medicine at Sunshine Hospital Melbourne, Dr Clifford Tan, Emergency Physician, GP and Toxicologist, Drs Mana Ittimani and Sam Bendall from Royal Prince Alfred Hospital Sydney and many more.

This two days of immersion into resuscitation. We’ve also added hands on workshops in ECG diagnosis, Xray and CT diagnosis and a procedures workshop.

This will be the most productive and beneficial two days you will ever spend. Join us at RESUS 2010. Click here to download the pdf.

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Rapid Sequence Intubation

Monday, December 14th, 2009

screen-shot-2009-12-14-at-83653-am

Practicing your technique at least every 6 months is very important if you do not regularly intubate. Even if you do, the ability to practice on different manikins and in different scenarios is very important.

In this video you can see a demonstration of rapid sequence intubation, as well as the correct use of the introducer and bougie. The positioning of the patient is paramount, as is the correct use of the laryngoscope.

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