Tag Archive: airway


The Rapid Sequence Intubation is one of those “gotta have” skills for clinicians who work in frontline medicine. Fair to say there are a lot of sequences out there, but they all follow the same basic plan – prepare, inject the juice, and get the airway secured ASAP.  In recent years there have been a few changes to the long-held anaesthetic dogma, based on good evidence.  So I thought I would take a look at a few, see what is new in RSI.

 Pre-oxygenation strategy:

In case you have been living under a rock and missed the Weingart & Levitan paper on Pre-oxygenation and Avoiding Desaturation in Emergency Airway Management here it is.  The practice of throwing on a Hudson mask at 6 litres/min for 5 minutes is no longer the standard of pre-ox we should be aiming for.   Weingart and Levitan have broken down the evidence and created a 3 tier risk-stratification of sick patients with incredibly practical strategies to optimise the pre-ox and decrease the rate of desaturation that inevitably occurs in the sick patients.

  • NIV as pre-oxygenation device – minimise the shunt, maximise the alveolar recruitment
  • Use of a viva-bag with a cheap PEEP vlave as a poor mans CPAP device
  • USe of high flow (15l/min) nasla cannula oxygen to keep the flow of oxygen throughout the procedure and make your apnoeic time much safer for longer.
  • Check out the tables on the last page of the above paper – it is pretty simple and self-explanatory

 

 

The role of cricoid pressure in emergency airway management has come under a lot of scrutiny in recent years.  As is often the case when we look back at the original data – it seemed like a good idea, had some experimental data to support it – but there was no good large-scale evidence that it made a difference to the outcome which we and patients care about!

There was a good review published last month taht asked the hard questions – in Trends in Anaesthesia and Critical Care 2012, Priebe looked at the data in a systematic manner and tried to separate facts from fiction.

In summary: 

  • Cricoid pressure does not have the evidence to make it a mandatory manouvre
  • Clinicians should use individual judgement to guide its use
  • It may be applied, and may help prevent gastric insufflation during BM ventilation
  • If your glottic view is obscured / inadequate – remove it ASAP, then consider BURP instead
  • There is a paucity of good, reliable evidence to support or deny the use of cricoid pressure!

 

There have been a few recent debates on the use of muscle relaxants.

  1. Should they be used at all in critical care settings?  For me this was a surprise, as I was trained by anaesthesia docs who always used them, but there is a tendency to avoid them in some ICUs.  If you want to hear the low-down on the debate in a very enertaining deabte go to Emcrit and listen to the Paralytics debate. Fair to say it has yet to be decided – but I think for the average GP-intubation it remains the standard to use a muscle relaxant.
  2. Which muscle relaxant?  Roc vs. Sux?   well there have been a few posts and opinions out there – check out my post from last year and links to other resources.
    • In summary – Roc seems to prolong the time to desaturation
    • Give it in a big dose ~ 1.2mg/kg and its onset is comparable to Sux
    • The “back out” plan that Sux ‘allows’ usually is not an option in true critical / emergency RSI
    • You don’y have to worry about the patient fighting the vent anytime soon if you use Roc!

 Last point – The PPPPPPP rule [proper planning and preparation prevents piss poor performance]

Having a well thought-out team-orientated approach to emergency airways is the most important thing to do to make your RSIs go well.  This should be done as part of your departments training / drills and education programme.

Dr Tim (KI Docs) has sent me this nifty little aide-memoir to help get your preparation right and to jog one’s thoughts with asimple checklist included.  I will put it in the Resources section at the bottom of the blog, but click here to have a look at the RSI DUMP kit mat.  Print it out in A# or bigger and put it on your resus room trolley.  Thanks Tim

Let me know if this helps – or if you have other new pearls for the old RSI setup.

Casey

I caught this audio last week at about 4 AM when the ambos rushed this 3 1/2 year old boy in with his mother to ED.  The story was classical croup – a day of URTI sxs, coryza, low grade fever followed by the early AM wake up with stridor, the “seal barking” cough and marked dyspnoea.  So it was a slam dunk for diagnosis.  Also the medical students never get to hear a good croup bark – because they are always safely tucked up in bed at 4 AM – so I produce this video to share….Croup (click to view)

Now this kid was sick:  RR 60, marked chest wall recession, biphasic stridor and looking very scared.  Of course his SpO2 was 99% – as it often is in early, severe upper airway obstruction.  The Ambo team had given 2 x salbutamol nebs in transit without any change in his dyspnoea.

On examination his chest was ‘clear’ aside from transmitted stridor.  No wheeze, creps etc.  So it had to be croup.

Given how severe his dyspnea, we went in with an adrenaline neb immediately – which worked really well – he lost the stridor after 5 minutes and his work of breathing improved dramatically.  We got an IV access and gave a dose of oral dexamethasone. Yes, I use dexamethasone – not prednisolone.  I guess you could argue for IV hydrocortisone – no problem with that.  I do not use prednisolone for the following reasons:

  1. It tastes terrible, whereas dex is sweet and kids tend to swallow it better
  2. The trials done right here in WA used dexamethasone – see Geelhoed et al these trials showed in summary -
    1. Paed Pulmonology 2005:  0.15 mg/kg of oral dex was as good as 0.3 mg, and 0.6 mg in treating croup
    2. BMJ 1996.  A single dose of 0.15 mg/kg dramatically reduced recurrence / representation in mild outpatient croup
    3. Arch of Dis in Childhood 2006.  Dexamethasone as above was superior to prednisolone in preventing recurrence and other markers of severity for managing mild – moderate outpatient croup.
  3. Prednisolone has some mineralocorticoid activity which is just unecessary in this clinical context – dex is a bit cleaner.
So anyway back to our kid in ED.  He settles with the adrenaline, the dex has time to kick in and he looks like a mild croup and hour later – the sun is coming up, so the paraflu is running back to cover!  We admit him to the ward and ask the friendly Paeds to review him on their round.  I head off to bed…
Around 10 AM I stumble out of the on-call room and pop onto the ward to check on the little guy.  The Paediatrician says:  ”Oh that kid isn’t croup -he has asthma!  He has a good going wheeze and is responding to salbutamol…”
So I say: “Nah, mate.  He was croup – classic!” and I show her the video clip above. We agree that we are both right.
Back the truck up and look at the previous history – there was a strong family history of asthma / atopy, smoke exposure and one possible previous episode of asthma after a viral illness. So – he probably has another bout of viral-induced asthma, the virus [maybe paraflu]also caused the croup.  Of course the adrenaline neb did a great job of masking any wheeze / bronchospasm signs he might have had.
1. There can be 2 disease processes taking place in the same patient.      2. Examine, then re-examine kids before and after interventions      3. After an emergency – you still have to go back and take a thorough history

 

The winter in Australia is at an end, which means we hope we have seen the last of those wheezy, crackly, sick looking babies for the moment.  Bronchiolitis is the bread and butter of a lot of Paeds wards and EDs over the winter, we all know how to diagnose it and what the normal course is.  But I think we are mostly treatment nihlists.  My teaching to the JMOS and students has always been simple – keep them in if they are small, sick or have unreliable carers; keep them hydrated;  and give ‘em oxygen to relieve their dyspnoea and try to normalise hypoxia.  However – I fear I am a bit outdated – maybe too simple…

There have been a heap of trials and reviews in the last 5 years looking at what might work in bronchiolitis - and what doesn’t.  So I thought I would do a quick review of the literature and find out the evidence circa 2011….

So what works?

Nope.  Cochrane review basically showed no consistent benefit in important outcomes – admission, length of stay..  There was a possible mild improvement in clinical severity scores in children treated as outpatients in some studies – not sure how this translates into practice.  There is a risk:benefit[side effect vs. mild improvement with B2agonists] trade-off, so bronchodilators are at best unhelpful on balance.

Yes, it does according to recent studies and the Cochrane analysis of the studies which all agree – it works.  If you would like a well thought out and detailed review of the literature – go to WA’s own EMPEM website and listen to Colin Parker (no relation) and his team go over the numbers. In practice this is an inpatient intervention, though you could use it in the ED.  The studies showed a decrease in the length of admission as the main outcome of benefit.  Check out the NNT review on the topic for more info

For me this is the big new thing in bronchiolitis – so cheap and easy, the evidence looks good and I think this is practice changing for our hospital – any comments?

HArd to say, the NEJM published this study in 2009 looking at inhaled adrenaline and high doses of Dexamethasone orally – the jury is still out.  I have heard a number of doctors interpret this study in a number of ways – it looks promising, but then the fine print taketh away.  The dose of dex was 1mg/kg (big), and the use of inhaled adrenaline is not always a fun intervention – so big guns were used and the benefits were mild if there.  Don’t tink this is going to change my practice.  If used – I think it is in the ED, the goal being to prevent admission – I cannot imagine the ward staff being happy to do this outside of a well monitored bed.

Well – not a lot of data. Only one true RCT to look at it. In my experience a lot of kids get them – but no good improvement. So – no, I never have used them in the straight bronchiolitic, and I still won’t.

Well – not a lot to go on – it did improve PaCO2 in this study, but not really a patient oriented-outcome sort of way.  This seems to be the cool new thing for the little ones with bad bronchiolitis.  I have little experience with it, so we will see…

This has been shown to help in asthma. But in bronchiolitis – this large international study was clearly negative

Well – we saw the mixed results from the dex/adrenaline trial out of NEJM in 2009. Was there any other evidence for roids? The Cochrane group looked at the big trails and found no benefit.

So those are the interventions we as Docs have looked at and tried.  Traditionally there are few interventions that help other than a tincture of time and watchful waiting.  My review has shown me one possible addition to the armament – super salty nebs seem to be helpful.

Anyone out there got any other tricks they use in the bronchiolitics?

Casey

 

All of these recent posts and commentary on severe COPD has lead to a few discussions about the management of the Acute Severe Asthmatic around my workplace.  It is fair to say that this is an area where tradition and long-held beliefs have a grip, but there is a bit of recent evidence to suggest we have some options with good efficacy which we should use in this nasty disease of largely young people.  So I have had a look at the evidence and reviews and come up with my usual super-summarised version for the simple folk like me to read…

Oxygen is good. Give it. No evidence, just do it.

In Australia this is salbutamol [albuterol in the US]. This is proven to be effective and reduces hospital admission / physiological parameters etc. There is a Cochrane review looking at continuous vs. intermittent nebs which showed a modest benefit to continuous vs intermittent nebs.  So how does this change my practice?  In reality we give nebs, and give a lot, so just give as many as you can probably no downside to continuous and in practice you will have gaps, ce la vie.  I think you need to be aware of the side effects – watch the K+ and heart rate, try and keep it as normal as you can.

In Oz this is ipratropium.  The evidence here is less convincing.  The summary from the Cochrane review – adding anticholinergics to B2-A in severe asthma is as follows:  A single dose of an anticholinergic agent is not effective for the treatment of mild and moderate exacerbations and is insufficient for the treatment of severe exacerbations. Adding multiple doses of anticholinergics to beta2 agonists appears safe, improves lung function and would avoid hospital admission in 1 of 12 such treated patients.   

So I say – go for it, give multiple doses of ipratropium to the severe asthmatics. Anecdotally it causes less tachcardia, and appears to have little downside.  But don’t settle for just one neb – I have been guilty of this I fear.

Steroids are well proven and part of the woodwork when it comes to asthma of all severity it seems.  In severe asthma they are given IV usually – hydrocortisone or methylpred.  The NNT is about 8, so well worthwhile I reckon.  Most of these patients get a guernsey on the ward – so how much steroids becomes a question for the ward team to ponder.  Turns out some is as good as a lot according to the Cochrane folks:  equivalent of 400 mg hydrocortisone per day was adequate with no benefit to higher doses.

Also some evidence to say early steroids might reduce admission – so give them early (first hour) and you might save a bed’s occupancy (not my favourite end-point)

There are 2 Cochrane reviews on this – one for kids and one for adults and the data turns out to be about the same. In practical terms aminophylline seems to have some effect on bronchodilation but no difference in the patient-oriented outcomes of – intubation, mortality or symptom reduction. Aminophylline has a narrow therapeutic index and high rate of side effects- eg, vomiting [which is even less fun when you are in respiratory failure and you might inhale a carrot] So the jury is tied but not moving anywhere – I think I will give it a miss unless everything else has failed, even then, not a good drug to give to an already super-sick patient.

Magnesim keeps popping up everywhere it seems. So in severe asthma – what is the deal? Well magnesium looks very good for severe asthma – the NNT is 2 – 3 for “admission”! Nothing is that good in our day-day work.  Once again – this end-point is a bit shaky – I am going to admit them anyway if they are severe enough to need Mg, however there was no documented harm – so I think I will keep doing it. How much do you need?  I used the same dose we do for eclampsia – are there any guidelines out there?  This recent Brit study also showed Mg (thanks resus.me) was good at limiting tachycardia in these patient – which is a bonus given how much B2-agonist we are using – has to help the CO a bit to keep the HR down?

However beware – no benefit found for less severe asthma – so this is easy – if they are not sick enough to get a drip, don’t give IV mag.

There is some evidence for nebulised MgSO4 – in this review it improved pulmonary function but not clinically important outcomes – admission, symptoms etc

Giving iV salbutamol is one of hose things we do in bad asthma, but is it a good idea?  Well, maybe not.  The best review I could find was 10 years old and showed no benefit, some worse physiology and lets face it – it makes you feel pretty crappy.  Positive chronotropy plus increased O2 demand seem like bad things in asthma.  So I think I will leave this out until further review.  Kane from LITFL has reminded me that an adrenaline infusion is worth a try in the severe asthmatic not getting better on all the rest – probably OK in place of salbutamol – works on the same receptors – any evidence – not sure….

Now we get to the meat of the matter. This seems to divide ED folk.  The teaching has for a while been – NIV for COPD but not for asthma.   So lets look at the evidence…  well not so easy, as there is not a lot of good quality data out there – no RCTs, only some case series and observational studies.  It seems very tricky to make a clear choice based on the available evidence as it is almost certainly biased by the fact that given the current culture only the sickest status asthmaticus patients would be getting a trial of NIV.  The Cochrane group looked into NIV and found it was proven to help with some endpoints, no different for others and negative effect – it depends which outcome you look at.  We need a good RCT on this.

In my opinion it would make sense to put a severe asthma with respiratory failure on NIV if you are planning to intubate otherwise – Scott Weingart @ Emcrit has posted on this a few times.  However, my understanding is that NIV works by assisting ventilation in the patient with respiratory muscle fatigue, and rising CO2.  So why not use it early in the severe asthmatic and prevent this from occurring as much as possible?  Is there a downside?  Sure you need to watch the preload and BP, but they are usually fitter from a cardiac POV than the average COPD patient with chronic lungs / pulm. hypertension and a bit of IHD from all the cigarettes.  So should we use it earlier – not wait until they are on the brink of intubation?

DrGDH has a new blog – he appears to be slightly obsessed with all things NIV – check out his posts on the topic – NIV in Asthma? no point right?.  Covers all the current available evidence in a page of internet – check it out.  The theme seems to be – lots of small, non-randomised trials that show a decrease in the need for intubation / IPPV in the severe asthmatics, but not enough good data to say for sure it works.  So – what to do?

I think it is worth a try, still need to do all the medical management, and I would definitely prefer a course of NIV if it were me!  In our little hospital I think this is a smart move – intubation mandates a long air transfer with significant risk.  After all – we can still tube them if the NIV fails – but once you have intubated – you have committed to a long, expensive and potentially hazardous transfer.

So once all else has failed – you have an otherwise healthy patient with respiratory failure and the end of the road if intubate and ventilate. Sounds good – but be warned – this is a tough road, ventilating a patient with this degree of obstruction is tricky. And you had better have a good plan for induction and getting the vent running – because a minute of fiddling might be the difference between a bad situation and a disaster. I am not the expert - Dr Scott Weingart at EmCrit has a great podcast on this scenario – so I direct you there for some gold! In summary:

  • Prepare, plan and plan B, C ready.
  • Have the patient on NIV for the induction – and have the vent set to go once you are in.
  • Use ketamine for your induction – it is a bronchodilator and keeps the CO up.  You might want to ensure adequate preload before switching to IPPV.

USe the “obstructive lung vent strategy” as per Dr Weingart

There are only 4 things you need to remember for an obstructive patient

  1. Vt (Tidal Volume) = 8 ml/kg, don’t mess with it
  2. Flow Rate = shorter insp times, 80-100 lpm
  3. Resp Rate = Lung protection, start at 10 work your way down if necessary
  4. FiO2/PEEP = Oxygenation, should need much O2 (40%)m I recommend PEEP of 0, but certainly keep it less than 5

Dr Minh Le Cong (RFDS) is possibly the most promiscuous blogshere lecturer out there – he pops up on all the best sites!

After playing the field at Emcrit and LITFL, he is back on Broome Docs this week covering our favourite topic – Psych sedation and retrieval.  This is his presentation to the Australian Aeromedical Society at Burswood in Perth, Western Australia last week.

Minh has sent me the link for the download as it is a big file – too big for this little blog.  So if you need a dose of Minh / ketamine check out his lecture at:

https://rcpt.yousendit.com/1214000281/1d760fcd7988cbbb786f1c799a58272a

It takes a bit to download, but is well worth it.  Then if you haven’t read my recent case on the topic – check it out @ Livin’ the Ketamine dream.  Minh tells me it is the first ketamine-based transfer of psychosis in WA, and might be the shape of the future if you follow Minh’s data from Queensland.

Enjoy

Casey

If you are new to Broome Docs, then you might have missed my mild obsession with Acute Psychiatric Sedation.  (GO back and read the posts from earlier 2011 to get the background and some tricky cases to ponder.)

Last night I had my first opportunity to put Dr Minh Le Cong’s secret weapon (ketamine) into action.  I had a large, schizophrenic patient who was very agitated and due to fly in an hour on the RFDS.  The patient had good going sleep-apnoea, a thick neck, big belly and a history of aspiration pneumonia during a previous sedation-gone-wrong.  This is one of those scenarios where you can make a bad situation worse without trying too hard.  So how did I manage this?

  1. Communication.  Get on the phone and make a plan with the flight crew.  We decided to try and avoid intubation if possible, this patient had a lot of co-morbidities and would not do well with a day or two on the blower.
  2. Team huddle.  Organise your own team, make it clear what the plan is and what plans B, C etc are.
  3. Move to the light => we moved the patient into the Resus area, fully monitoring (including ETCO2) and had the airway gear all ready to go
  4. Sedation.  Titrated sedation is the only way to go.  Give a dose and watch for a bit – chronic Psych patients have a wide range of tolerance to various drugs – so don’t just use a pre-formatted recipe – you have to give a bit and observe response, then repeat. As previously stated – I do not see why a Psych sedation should be done in a low-acuity area, where we would never do procedural sedation for a surgical problem.
  5. Change the plan if plan A is not great.  This patient got quite deep with 4 mg of midazolam and required a nasalpharygeal airway.  So I changed the plan – ketamine.  This worked well – RR went up a bit, patient  was tranquil and allowed us to site another IVC and an IDC with minimal fuss.
  6. Bedside vigil.   You need to be nearby to monitor this patient – you cannot give drugs and wander off to other areas.  I stayed around and actually went with the patient to the airstrip to ensure the plan was working.  Maybe once we are all more familiar with these agents in practice we can relax a bit, but for now I plan to keep my eye on them.

At the end of the night all was well. The patient was sedated, but rousable, moving herself on the stretcher.  Nobody got punched or spat upon.  The RFDS crew seemed happy and her numbers remained perfect throughout.

Winter in any paediatric ED means – flu season, bronchs, croups, URTI etc etc.  It can be tough to pick the true sick kid out of the haystack of cranky, viremic ones.  This case illustrates this point beautifully!

10 month old girl with a classic story – URTI sxs for 2 days, then woke at midnight with a harsh / brassy cough, hoarse / weak cry and stridor… too easy:  croup.  Presents the next AM to ED.   Tired looking mum is happy to take her home and try a dose of dexamethasone this evening.  (See a couple of studies to support this from NEJM, Bjornson [0.6 mg/kg]  and our own West Aussie Gary Geelhoed, PMH in the BMJ [0.15 mg/kg]).

So I saw this kid the next day, had tried the dex and was not much different, rough night, harsh cough, but looked better by sunrise.  On examination – snotty nose, red throat, chest clear, no stridor, OBs all OK, low-grade fever.  My thoughts – likley this is croup, she was just a bit smaller than the average croup kid, so needed another day / more dex to get her through.  No story or signs to suggest a FB.  So I sent her home with another dose of dexamethasone, return if the stridor returns / increasing distress etc….

I was expecting to see her again (if at all) around midnight, but no…  3 hours later mum brings her back – stridor, fever, marked chest wall recession… hmmmm… not how croup should behave.   So we tried the dose of dex she was going to have later, and watched her closely.

I think this is a crucial point in Paediatric decision-making.  We see a lot of  “syndromes” of common illnesses (asthma, bronchiolitis, croup, gastro, otitis….) and we “know” these well.  Recognising a variation from these patterns is a vital clue when trying to spot the sicky in the viral haystack.

 Back in ED – I was called away to gas an ectopic.  Halfway through the case I got a call from my colleague – she is not doing well, working hard and stridor worse, fever spiking.   So we went for the adrenaline neb (Cochrane Review of Adrenaline in Croup - “it works, for a while”), which predictably helped.. for a while, then she became dyspnoeic again, so another round of adrenaline was given and a call for help went out!  We were in trouble.  I do a bit of Paeds Anaesthesia but tubing a 10 monther with an oedematous airway is not in my repertoire usually!

Bacterial tracheitis   (Staph / Strept) is most likely in a vaccinated child. Consider epiglottitis in a kid from overseas or non-vaccinated for Hib.  Other rareities: tumour, vascular malformation, retropharyngeal abscess, FB.

 

There is no good answer. I have asked a number of Paeds Anaesthetists and gotten a range of answers. Spont ventilating gaseous induction? Nasotracheal intubation?  Controlled RS intubation post adrenaline neb ? Äwake fibre optic” = impossible in an infant.  What about ketamine? 

Please tell me, how would you do it??

If you are a reader of our comments sectio, you will know about Dr Minh Le Cong – RFDS Doc from Cairns who is one of the most enthusiastic teachers I have come across in the ether.  If you want a sample of his pearls of wisdom – go to my post on Preoxygenation Pearls and check out the comments section.

One of his passions is teaching airway skills to GPs / occasional intubators.  He also loves debunking medical mythology and dogma – and he has taken aim at the classical Rapid Sequence Intubation (RSI) and cricoid pressure.

So if you are an occasional intubator, or just would like to know what all the controversy is about – Minh has allowed us to put up his lecture on the topic.

The Occasional Intubator for Broome Docs blog

Check it out  – let me, and Minh know what you think.  I am sure there are some Anaesthetists out there who have something to say?   Casey

Now this is a huge post, apologies in advance – goes a bit over the usual 2 minute read I aspire to!  But… this is gold.

Ever been in a “Can’t Intubate, Can’t ventilate” scenario  - if you said ‘no’ then lucky you.  It is a rare occurrence in Airway management but one which has a very high mortality – and sadly often the harm is iatrogenic, ie. our fault.

In my career I have witnessed one true CICV scenario when in training and it scared the pants off of me.  If you want the details they are a matter of public record in the Coroner’s Findings into the death of Rachael RASMUSSEN. (FYI the Dr Casey in this report is not me)    I was a “fly-on-the-wall” trainee that day and saw some great Anaesthetists struggle with a CICV scenario which was entirely avoidable.

Since then I have been involved in 2 emergency surgical airways and which have gone well, mainly as a result of the training my colleagues and I have undertaken after having our pants scared off.  In my opinion, this the ‘Elephant in the Airway’ that nobody is talking about.  We all know that surgical airway is down the bottom of the difficult intubation algorithm – but how many of us are confident enough in our training and decision-making to make the best of such a disastrous situation?

Here in WA we have a wonderful training facility based at Royal Perth Hospital which has done a lot of research into the CICV scenario using wet-lab simulations on sheep.  Dr Heard and his team have published their CICV Algorithm based on the experience derived from hundreds of trials using anaesthetic trainees (the sheep were the ‘guinea pigs’, not the trainees – excuse my Irish logic).

Anyway after spending a bit of time debating my preferred Surgical airway technique with my colleagues I decided to get the low down straight from the horse’s mouth (way to many animal puns in this post) and do an interview with Dr Andy Heard.  Here is the proposed algorithm from Dr Heard’s paper from Anaesthesia, 2009 for your reference.

To answer this question in full would require two pages, but I will be brief. My algorithm has been developed primarily as a plan for airway specialist trained in anaesthesia. Ultimately the skill mix of other groups may well mean that they would be better attempting a different path. E.g. an ENT surgeon should use a scalpel blade. Which approach is appropriate would be a decision for the individual. Note that NAP4 surgical techniques were often performed by specialised airway surgeons with all the theatre backup they would be used to. No technique is infallible; our algorithm encourages a systematic progression through techniques, with the pathway moving from cannula to a scalpel technique if required. I would recommend that you are prepared for all eventualities i.e. familiar with both cannula and scalpel to allow you a better chance of success. If this is appropriate, then a cannula technique performed along our guidelines does not cause major difficulties with scalpel techniques but a scalpel technique that fails but causes intra-tracheal bleeding unfortunately makes aspiration of air as an end point very difficult and leads to cannula failures which would have been successful. Ultimately there are a lot of requirements for successful management of this scenario: teaching, training, equipment availability etc. which can also affect your choice. I can add that we have regular E.D physicians coming through the wet lab, at least 2 of whom have successfully saved a patients life with a cannula technique and then secured the airway with a Melker.

(2)

This is actually a similar question to number one. An (our) observational study on success is no guarantee of success. These were all on easy necks with easy to palpate anatomy. Performing a scalpel technique with no identifiable anterior neck anatomy is inherently far more difficult and not appropriate for the scalpel bougie. I occasionally have people attend the wet lab and say that the scalpel bougie is their “take home” choice. I point out that if that is their plan, probably in 1/3 of patients they will not be able to proceed due to difficult anatomy. You can proceed with a cannula no matter what the anterior neck airway anatomy. Part of the problem, in anaesthesia at least, is that speciailists struggle to make the decision to go round the front of the neck. Giving a simple choice, with no decision process required of a cannula first every time encouraged people to attempt rescues oxygenation through the front of the neck. This reluctance is well documented in critical events (e.g. Elaine Bromiley). They can still move onto a scalpel technique if required.

(3)

Again requires a long answer. But put simply we have pointed out for many years now that most of the anterior neck airway equipment “designed for purpose” is unreliable and often unsuccessful in the emergency situation. Hence we have rewritten the plan, techniques and changed the equipment to suit the requirements of the CICO scenario. NAP4 has often very nicely validated our points in regards to this. Also many (if not all) of the surgical airways using a scalpel were completed by surgeons (in particular head and neck surgeons), not anaesthetists. They also point out that they may have missed many events, including successful cannula that were not reported. There were no recorded details of operator experience or training. Emergency airway management through the anterior neck is not something we do every day. To try and use an analogy – If we were to advise all surgeons to use a laryngeal mask (which they had never used before) and asked them to use them for the first time in anger in the worst airway scenario of their life, the results would not be reassuring; in a NAP4 equivalent study looking at airway disaster for surgeons. If interpreted as NAP4 seems to be interpreted against cannulas, it would convince surgeons to never use a laryngeal mask in an airway emergency. If they also audited anaesthetists who used laryngoscopes then they would say that laryngoscopes worked very well and hence all surgeons should just switch to using laryngoscopes. This would not improve their outcomes, but would end in disastrous results. Even with some training you do not gain satisfactory laryngoscopy skills easily on a manikin. What they would need is training in the technique which suited them, using appropriate equipment. Looking at the surgical “High success rate” that they compare against the cannula low success rate. Only 11 of the scalpel surgical airways were true emergencies in NAP4, and of these 2 patients died. This is with surgeons who know how to hold and manipulate a scalpel blade, have diathermy ready and know how to use it, are in their relative “comfort zone” i.e. using a scalpel not a cannula and in many are airway surgeons who do incise the neck every day of their working life. If this is to become the gold standard for all airway specialists how are we ever going to teach everyone to manage this situation? I suggest the only way would be for all airway specialists to have to undertake at least 1 year of ENT training. We purposely moved away from standard scalpel techniques in our plan for a variety of reasons, one as stated to allow a direct path onto the algorithm to avoid decisions and fixation errors, and secondly because our, now quite extensive, experience of scalpels held in anger by anaesthetists and other specialists in the wet lab showed very poor results. This has been addressed in some way by the scalpel bougie technique which minimises scalpel manipulation and hence scalpel skills, but this technique is only appropriate if the airway anatomy is palpable. Trying to give anaesthetists or other specialists the skills to manipulate a scalpel in anger in a stressful environment is a virtually insurmountable task. One final comment is training also needs to switch from the ongoing plan of ventilating through the cannula to accepting oxygenation is the priority and ventilation is secondary. The cannula is only a temporising measure to prevent death from hypoxia whilst working out your next step (See algorithm). NAP4 lists cannula failures, but some of them are surely jetting failures due to poor jetting plans and technique. Having a safe plan for this is essential, and we are currently publishing our latest on this.

(4)

There is some evidence regarding recall and hence requirements for ongoing training, one that comes to mind is Wong et al from Canada published that study showing that on a manikin it requires 5 practices at cannulae to get the technique correct… and that they recommend retraining every 6-9 months since this is the time period for deskilling.. All airway specialist do not need to attend a wet lab for training. Attending a training program that teaches a plan and techniques that are well thought out and logical is the first step. The algorithm and techniques I have developed are now taught around Australia, on NATCAT, at Airway SIG meetings, AAMRC in Melbourne, WAAG meeting and wet and dry labs here in WA, Also in Brisbane on Keith Greenland’s course and in Adelaide on Chris Acott’s courses. Also To encourage and help with ongoing refresher training we have put a set of videos on yotube to allow people to refresh their plan. Look for drambheardairway on youtube.

(5)

This is a scenario that was faced by a G.P. anaesthetist who had attended our wet lab training to return to the Kimberley region in WA and end up having to perform a surgical airway on a colleague for just this reason 3 days later. He initially (successfully) put a cannula in and then was going to convert to a melker but realised his hospital at that point did not stock the melker kit. He, having had experience of the EMST technique in the past which had not been altogether positive, went on to do a scalpel bougie, after removing the cannula and secured the airway with a 6.5 CETT. Having performed many ICU transfers in the UK, admittedly mainly by road but often very prolonged, I am of the opinion that securing a cuffed airway is of major benefit to the patient. It will always be scenario specific, but either cannula or scalpel technique can be attemped. Looking at complications, one of the major issues with cannulas, I accept, is the attaching of high pressure oxygen to the cannula to oxygenate the patient. In this scenario there is no requirement for this and you can just perform a control melker insertion without jetting or time pressure. This is the ideal scenario for inserting a melker as there is no time pressure for success and you don’t have to jet down the cannula hence avoiding barotraumas issues.

(6)

I just had a paper published recently in the European Journal of Anesthesiology on this topic. If U/S is available and you are having difficulty identifying the anterior neck airway anatomy then definitely it is worthwhile We showed that in a time pressured environment, if the trachea was not midline, U/S significantly improved performance. In this day and age of U/S becoming ubiquitous in many critical care areas this is certainly going to become more used. If nothing else ensuring the trachea is midline prior to induction, or an X marks the spot, is worthwhile if you have time.

 

In the 14th century, French philosopher Jean Buridan was satirised for his philosophy using the paradox of “Buridan’s Ass”.  The paradox involves a donkey who is standing exactly midway between a bale of hay and a bucket of water.  The donkey dies of both starvation and thirst whilst inconclusively trying to decide on a logical course of action.

How is this relevant?  Well I think that the real problem with surgical airways is the “option paralysis” that takes hold when one finds oneself in a CICV scenario.  If you have not thought it through or practiced a solid, reliable (in your hands) technique. Then your patient may go the way of the aforementioned donkey.  I am sure there is no single, perfect surgical airway technique, but you have just gotta have a “go to” technique for when the situation arises.

With all the recent posts about sedation in Psych and agitation I thought I might take a moment to draw your attention to the recent White paper from ACEP about the syndrome that has come to be known as Excited Delirium.
This syndrome has been described in the literature for 150 years!  Only recently has there been an effort to formalise the symptoms into a treatable syndrome.  Some of the cases that have come up during the discussion could easity have been included under the desription of the syndrome – see Case 011 or the coroners report into Mr Fernandez in Qld 2005.
What are the basic features?
  • male subjects, average age 36
  • destructive or bizarre behavior generating calls to police,
  • suspected or known psychostimulant drug or alcohol intoxication,
  • suspected or known psychiatric illness
  • nudity or inappropriate clothing for the environment
  • Tachypnea, sweating, tactile hyperthermia
  • Pain intolerance – often struggle after Taser or pepper-spray
  • Obesity is a common finding in these cases
  • failure to recognize or respond to police presence at the scene (reflecting delirium),
  • erratic or violent behavior, often towards inanimate objects
  • unusual physical strength and stamina,
  • ongoing struggle despite futility,
  • cardiopulmonary collapse immediately following a struggle or very shortly after quiescence,
  • inability to be resuscitated at the scene, and
  • inability for a pathologist to determine a specific organic cause of death,
So is this a true “disease” or just the end point we see when patients on a catecholamine surge develop hypoxia and crash with severe acidosis?  This is the point of a lot of debate – some say it is the Taser that kills them, others the Police restraints, who knows.
What we do know is that these patients have an ominous tendency to crash and arrest almost without warning just seconds after “giving up the struggle”.  A brief period of quiescence followed by cardiopumonary arrest has been well described throughout the literature.
So how will this change my practice?  Well I think I ahve already stated my preference for doing sedation in a well controlled / airway ready environment.  I reckon this syndrome will make this conviction even stronger.  Beware the speeding/agitated patient who has just wrestled his way into the ED in Police custody – the urge to sedate is  strong… but just be ready to do a full ABC resus before you jab in some IM sedation!
    Has anyone out there seen something that meets this description?  Please share..