Tag Archive: oxygen


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

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.

This post might become a regular under the banner “What I learned from Scott Weingart this week!”  Scott runs the EMCrit blog and if you haven’t seen it – do yourself a favour and download his podcasts from Itunes – he is a great teacher, and pitches his education in a practical / pragmatic fashion that is well suited to rural GP Anaesthetic / ED types.

I got in contact with Scott a few weeks back to give my 5 cents on “pre-oxygenation”, basically I (and a lot of Anaesthetists) was taught to think of it as “denitrogenation” of the lungs – aiming to get the ET O2 up to 80 – 90% prior to RSI.  This is true, however as Scott has pointed out in his video response – this is missing a few crucial steps.  You cannot directly translate what we do in OT back to the crashing ED patient.

Check out Scott’s video and demonstration of pre-oxygenation on himself.
Then check out Scott’s “DSI: delayed sequence intubation” concept – this is basically how to preoxygenate a sick patient, and hopefully avoid them crashing on induction. The link then links to another video demonstrating the technique.

This is me learning a better way, it does break a few of the “Anaesthetic Commandments”.
Would love to hear your comments
Casey

This case happened today and I think it is in my top 3 ventilation challenges ever!

19 yo man, fit and well, thin.  Acute appendicitis, not particularly septic pre-op.  Underwent routine RSI and  open appendectomy (necrotic appendix, no free fluid).  muscle relaxants reversed and extubated without incident and moved to Recovery room.   About 10 minutes later was noted to make a long ” groaning noise” and rapidly became hypoxic.  Commenced BMV by GP anaesthetist – easy to bag – SpO2 low – 60 – 70%, no improvement after a few minutes, lung sounds “wet” bilaterally.  I came in at this point as a second pair of ands – we decided to return to OT and reintubate.  Working diagnosis at this point was “negative-pressure pulmonary oedema” following a probable episode of laryngeal spasm (possibly aspiration-induced).

Patient was re-intubated and sedated.  Commenced on Vol conrol with PEEP 10 cm, SpO2 improved to 90% on FiO2 98%.  POrtable CXR = diffuse, bilateral ‘fluffy’ perihilar infiltrates.  Small right upper lobe consolidation.

At this point we decided to keep going with PEEP and plan to attempt to wean it down over the next hour or so if possible, given frusemide and art. line inserted.

ABG – pH 7.22, pCO2 – 66, pO2 – 60,  on 100%.  At this point it became clear we were dealing with serious lung injury.  Patient coughed and pink frothy sputum coming up the ETT.  SpO2 started to decline over the next few minutes.  We re-paralysed and took control of the ventilation.  The plan:  set a smallish Vt (6ml/kg), high RR to ventilate and bring CO2 down,  increase PEEP with intermittent prolonged PEEP “recruitment” manual bags.  This was effective and the SpO2 came up again to 95%.  However over the next few hours the patient became increasingly hypoxic.  Airway pressures were rising, repeat CXR showed worsening infiltrates, no pneumothorax.

By sundown we were running PEEP at 18 cm, RR – 22/min, Vt = 425mls.  BP started to drop, we put in a CVC and started some Norad – central pressure and IVC index suggested patient was well loaded, reasonable urine output.  We were not keen to increase PEEP further and the hypoxia once again increased – Sp)2 consistently 84%.   What to do…?  We needed to get this guy onto the Oxylog 3000 at some point also as the RFDS were incoming to fly south.  One attempt to change ventilators resulted in worsening hypoxia.   So…..

We decided to roll the patient – tried right (worse) side down – SPO2 much worse -75%.  So we tried right-side up – bingo, good improvement over 10 minutes = SpO2 up to 94%, We were able to start winding back the PEEP and successfully changed to the Oxylog.  2 hours later we were back to 10 cm PEEP and FiO2 of 0.50 on the Oxylog – the retrieval team were happy.  Patient was transferred south and extubated the next morning.

I would love to hear your experiences with this type of case, what would you do differently?

Check out the links below to some great resources for the tricky-to-ventilate cases:

From EMCrit this simple 2-strategy approach to ventilating the difficult lungs

Another paper looking at a few cases with references:

Another case discussion paper,

As you can see apart from case reports there is not a lot of “evidence” as to how to manage this phenomenom “NPPO”.

My reading of it is basically:  diagnosis is pretty much clinical with a good history of upper airway obstruction leading to rapid “wet lung”, you need to rule out other potentials – APO (cardiac), aspiration, PE, maybe fulminant pneumonia or tamponade??  Sometimes it is unilateral – esp. if the tube went endobronchial (doh!)  Early management includes oxygen, ventilation using PEEP and consider the differentials.  Lasix might help, but no evidence really… thinking outside the box, as a keen altitude trekker – would dexamethasone or Ca-cannel blocker help – they are used for HAPE in the Himalayas??  Watch this space..