Reframing Anaphylaxis; Roadside to Resus

So hi and welcome back to the Recess Room Podcast. I'm Simon Lang. And I'm Rolf Fenway. And we've got no James Yates, but this is our new episode of Roadside to Recess, I know, I know. Dry your eyes, mate. It's our new episode of Roadside to Recess and this time it's on reframing anaphylaxis.

I know, I'm so sad. James Yates was desperate to come on this episode, but he's off doing obviously very, very important work in whatever he's doing and uh we will be back next month, I believe. It's been so long since we were all together. But anyway, I I'm sad that he can't be here. I'm very glad that you're joining us. And yeah, we've got a great episode planned in terms of reframing Anaphylaxis.

And you know, I think that the important thing to say here is there is some new concepts coming out of the evidence and I am super pleased we bring in it and not only us, we have got a third member of the team this month. We've got an interview with a subject matter expert, haven't we?

We have, we absolutely have. And you're right, James is off doing stuff for a good cause, but I'm not sure that being sat on your bike is uh, you know, really a valid excuse to be off not recording on the podcast. But there we go. Someone's got to hold the fort, haven't they? Indeed. Before we get into it though, a huge thanks once again to Zol Medical Corporation for collaborating with us on the podcast and making this all free, open access and available to you.

In their pursuit of excellent patient care. And when you've listened to this, as we always say, hop over to the website and get your free CPD certificate for listening to it. So, got some great content in here, so let's crack into the episode.

Okay then, well anaphylaxis, something which I think If I know our listeners well, Simon, most of them will understand really well. They have seen this out there in practice, they've got it drilled in. We've done an episode on this before. It's simple, recognise, give that adrenaline, treat it all fairly straightforward. And that is because in most cases of anaphylaxis that is absolutely true. But of course, deaths do still occur out there, don't they?

They absolutely do. And I think this is a really interesting episode because as we're going to come on to the definition of anaphylaxis, a bit about the pathophysiology, a bit about how we conceptualize it in our mind. This is possibly going to challenge some of those aspects, especially those in the pre-hospital and in the emergency care setting. So yeah, it is fairly common. There's varying data on it. Some data suggests around one in 300 people will experience anaphylaxis in their lives.

and a fatality rate of one percent in those presenting to UK hospitals. Now fatal anaphylaxis is most common in children and adults up to the age of thirty years old due to food, and then in the elderly it becomes more common that those fatal episodes happen as a result of drug. Yeah, absolutely. And these numbers are amazing every time you read them because you see so many of these cases that respond so positively, don't they, to those treatments that we've mentioned already. But

After reading some new evidence that was sent through to me, there is some really interesting stuff out there. There are some new concepts that are challenging that idea. And the key question for me coming into this episode is, and the whole reason for us sitting down and talking today. Is are we thinking about anaphylaxis in the right way? So stay tuned because there's some good stuff coming.

There absolutely is. So we're gonna start off as we do thinking about definitions. And I think there are a few challenges when you look at the different definitions that are out there, because there is a bit of variance. Now the World's Allergy Organization Anaphylaxis Committee defines anaphylaxis as a serious systemic hypersensitivity reaction that is usually rapid in onset and may cause death.

And they say that severe anaphylaxis is characterised by potentially life-threatening compromise in airway, breathing and or circulation and may or may not occur without typical skin features. or circulatory shock being present. Yeah, absolutely, Simon. Now the RCUK, so Resuscitation Council UK, so their definition is not a million miles away. So it's anaphylaxis being a potentially life threatening allergic reaction characterized by sudden onset.

and rapid progression of airway breathing and or circulation problems, usually with skin or mucosal changes. And the key features that they recognise are that sudden onset, that airway breathing or circulation compromise that is often associated with those skin features that we think of like flushing, urticaria, angiodema, but actually gotta be careful here because they might be absent in around 20% of patients that have anaphylaxia.

Yeah, and I think when we were prepping for this episode, and be reassured we do do some prep for them. We do do a bit. A bit, yes. Varying amount. This was a lot actually this month. Yeah, and I have found the back of the postcard that we scribbled it down on. But um but when you think about it, we're talking about a rapid A, B or C or altogether compromise.

Now that is quite wide reaching, isn't it? It is. So it's probably worth trying to delve down a bit more into the pathophysiology. So as we've said, it's an overwhelming inflammatory process. in which you get tissue edema and smooth muscle contraction in the airways. You can get fluid extravasation, so giving tissue edema and hypovolemia, and you can get a profound reduction in venous tone.

You can also, as if that wasn't bad enough, get depressed myocardial function and fluid leakage into bowels and smooth muscle contraction, which can give patients pelvic and abdominal cramps. So that's the pathophysiology, but what about the presentation? Well, in terms of those A, B, or C aspects.

Airway swelling. So things like tongue swelling, throat swelling, maybe subtle at first, voice changes, maybe some subtle strider, which clearly can evolve, get those breathing problems. So again, looking early at subtly increased work of breathing. Maybe a bit of bronchospasm, which can become much more extreme. You can get hypoxia, and clearly at the most severe end of the spectrum, respiratory arrest.

And then circulation and I think it's fair to say that in my mind this is probably where I frame the biggest aspect of that ABC collapse. You can get those patients presenting pale, clammy, presyncope, maybe a tachycardia, hypotension, but ultimately, in the most severe cases of anaphylaxis, those life threatening ones, cardiac arrest.

And Simon, I definitely agree with you there. I think that is where the big focus is currently and you know, all you need to do is actually look at some of the guidelines that are out there and where Anaphylaxis sits within resuscitation guidelines. It's generally under a cardiovascular collapse.

section rather than being under an airway or a breathing issue. So I definitely agree with you. And that's why I think it's really important that we consider the new evidence that's coming on that is coming in just a second.

Well hold your horses because before we get to the evidence, we're gonna go through a bit of the guidelines and what the accepted treatment is. And we're gonna look at the RC UK guidance and as you would expect in a really sensible approach that is an A to E approach. Now they mention in those guidelines that you should be giving adrenaline early. It's the first line treatment for anaphylaxis repeated at five minutes if no improvement.

Now it's given IM for the rapidity at which you can give it, there's no need for access, and it avoids the potential for making significant dosing errors, especially if you're not familiar with giving IV adrenaline. Now what I think would be really interesting is just to think for a moment, what is the trigger in your mind for giving that adrenaline? Because I think it's fair to say from my historic mindset, that's pretty much been when somebody is shot.

But remember, we're saying that these presentations come in a variety of different manners, and we're talking about an A, B, or C problem. So it doesn't just have to be that circulatory issue, but we'll come back to that in a bit. So they say in the guidance, if in doubt you give adrenaline, you give oxygen, high flow immediately and then when feasible you titrate it down to try and achieve normoxia.

You're gonna give fluids if they're shocked or if they've got a poor response to the initial adrenaline. Antihistmines Back in my day, used to be part of the standard treatment set for anaphylaxis, but it's not in there anymore, can be used to treat some skin symptoms. But clearly that's not addressing the life threatening aspect of the presentation. And the routine use of corticosteroids in anaphylaxis is not advised, but

you could consider it in refractory reactions or ongoing asthma. And I think again, when you think about the way in which you can present with anaphylaxis, we need to recognize the fact that there is a significant crossover in these presentations with asthma and anaphylaxis, especially when we know that twenty percent of these cases are not going to present with those rashes, which I think

Again, is one of those things that's really drilled into us. Look for the rash and then look for the A to C problems. They also say that there's a place for treating bronchospasm with bronchodilators. And the risk is, I guess, with a podcast like this, is that we are talking about a diagnosis, but putting ourselves in the position of treating that patient

We are treating what we're seeing in front of us, aren't we? So if we're seeing bronchospasm but we're seeing a rash, that doesn't mean that we're necessarily just going to go down one line. We're still going to treat both aspects of it. So we're still going to treat with adrenaline for the anaphylaxis. But still give those bronchodilators as though it could be asthma as well, because ultimately we haven't got a final diagnosis definitively yet.

Now they also go on the guidelines and it's fair to say I'm condensing this and skipping some bits over, but they also go on to talk about the refractory anaphylaxis definition and this is important to remember. So that's anaphylaxis, which requires ongoing treatment despite two adrenaline doses. And in this the strategy is then to get IV or IO access, if not already gained, to give a rapid fluid bolus.

to give low dose IV adrenaline as an infusion and along with airway management and ventilatory support. So you need to have either access to clinicians that can deliver critical care Or if you work in the pre hospital environment, be delivering the patient with pace but safely and with expert management to a centre where that critical care can be delivered.

Now, just before Rob goes into some of the new evidence that's available on the topic, Nice also have some great stuff on anaphylaxis and they mentioned that misdiagnosis is common. And we've already said that, haven't we? You know, this is a myriad of ways that anaphylaxis can present. There's a huge crossover with asthma. They mentioned that there's confusion with mild allergy, asthma and mimics of anaphylaxis.

And also, and we'll come on to this a bit later, the need for follow up and specialist referral because clearly we're trying to cover this. to be more familiar ourselves and hopefully help you guys as well be a bit more familiar with how we should approach these patients. But when we've had a patient with anaphylaxis, the ultimate goal is to try and avoid that happening in future. So follow up is really, really important.

Yes, indeed, Langers. That is super important to remember. Now I wanna bring us back here to why we're talking about this and revisiting this topic at all. Well I will be honest with you, Langers. I got lost down a little bit of a wormhole and that's what's led to this episode. Okay. So a good colleague, friend of the podcast, Tom Roberts.

sent us two amazing articles which were both published last year using cases from the UK National Child Mortality Database. And they were both authored by a group including John Covenney, Tom Roberts and different colleagues. And there was also a very recent paper just published by Ben Mackenzie, who we are very lucky to have on later as a guest.

speaker. But let me first of all explain a little bit about that wormhole I got lost down with these two papers. So essentially paper one, airway breathing or circulation failure in fatal food anaphylaxis. Now the authors Reviewed fatal pediatric food anaphylaxis cases from 2019 to 2023 to identify. Whether airway breathing or circulation compromise was the dominant problem prior to these unfortunate deaths.

Now there were a total of twenty four cases that were reviewed with seventeen included in the final analysis. So not huge numbers, but this is super important and the findings were absolutely striking to me. So Forty seven percent of cases had both airway and breathing compromise. Forty seven percent had breathing compromise alone and only six percent, so one of those cases demonstrated isolated cardiovascular collapse without any preceding airway or breathing problems. Now all

All of the children in this cohort had both food allergy and asthma. And the key message from this first paper. was that fatal pediatric food anaphylaxis appears to be predominantly a respiratory problem, with breathing compromise being the dominant feature prior to cardiac arrest. So whoa, whoa, whoa, I'm like, hang on a minute.

Not that cardiovascular collapse that me and Simon naively and potentially other people out there were expecting and more used to anticipating. But hang on for a minute.

There is also the second paper. So this one was pre-hospital care in fatal food anaphylaxis. And this one basically followed the chronology of deterioration in that pre hospital care phase for these cases. Now they included nineteen cases in their final analysis and the key findings here so in all of those cases Cardiac arrest occurred before the arrival at an emergency department. Okay, so this is a pre-hospital issue that we're dealing with here.

Now thirty two percent of those children were already in cardiac arrest when the emergency services were called. A further forty two percent were not initially in arrest, but had progressed to cardiac arrest before EMS arrival. And the median time from symptom onset to cardiac arrest was just a mere fourteen minutes.

I mean goodness me, that is pretty striking, isn't it? Now the adrenaline element, so the findings around adrenaline were also important. I just want to pull that out before we go on to discuss. So thirty seven percent of these cases received no adrenaline at all prior to arrest. Another thirty-seven percent received only a single dose prior to arrest, and several children, it's important to note here, deteriorated despite adrenaline and pre-hospital respiratory support.

So overall here you've got a paper, this one, that demonstrates that fatal pediatric food anaphylaxis characterized by this really rapid deterioration. This fast progression into cardiac arrest in the pre-hospital setting and a dominant respiratory compromise.

You know, and I thought this was like super interesting and definitely not what I was expecting based on my experience of managing these cases and what I had historically been taught. But actually if you go digging back into the literature I go further down this wormhole now, metaphorically, if you look at some of the older UK literature, there's some work by Pumphrey in the early two thousands looking at fatal anaphylaxis.

And there were already signals in there that food triggered anaphylaxis behave differently. So asthma, bronchospasm, progressive respiratory compromise were recurring themes in those fatal cases. And back in twenty nineteen, the World Allergy Organization actually published a paper essentially questioning whether our existing definitions of anaphylaxis actually reflected reality.

So they highlighted that almost a third of patients presenting with anaphylaxis had isolated respiratory symptoms and importantly that this type of presentation was increasingly being seen more and more commonly in fatal anaphylaxis. Now they even changed the wording of the definition itself, specifically stating that severe anaphylaxis may occur without circulatory shock being present. But I will be honest.

That completely passed me by. And I think now that has really changed. And now what we essentially have got is we've got these tragic but modern national data sets, for example, the National Child Mortality Database work.

that really reinforce and quantify those earlier observations. So I guess the question is, you know, where does that leave us now, doesn't it, Langus?

Yeah, so it's been really interesting running through this stuff because actually when you take those papers and you take those databases, actually it doesn't conflict at all with the guidelines, does it? But it just it just for me Maybe this is showing my age, but it just for me shows that I potentially need to reframe the way I think about anaphylaxis.

And probably need to really change that trigger point at which I think I'm dealing with an allergic reaction as opposed to dealing with anaphylaxis in front of me. And we probably need to think about our thresholds. for using those different treatments that we've talked about in the RCUK guidance and the other bits that are out there.

Yeah, I definitely agree. I think the issue for me is that from my perspective anyway, I feel like there has been an absolute gap exposed in my knowledge of anaphylaxis here. And it doesn't say that I've been managing them incorrectly all these years.

It's just that I was unaware that this element of it was such a problem, you know. And I think that's what we're trying to get across here. It's not saying, Oh right, anaphylaxis isn't a circulatory problem. Well of course it can be But just that in the subsets of patients where there are more pressing priorities than that and we can't wait for those circulatory problems to develop before we look to intervene.

So clearly this has brought around some questions for us and having a subject matter expert would be a huge bonus and that's exactly what we've got because we've got Ben Mackenzie, who Rob was lucky enough to catch up with, and tragically Ben's son, Max. died from a hypoxic brain injury secondary to asthma, which was precipitated by anaphylaxis.

Now following this he's committed to helping us all prepare for similar cases that we might encounter in our practice an unbelievable legacy to leave to Matt. So Rob's caught up with him. Let's have a listen to those two having a chat about anaphylaxis.

Ben, thank you so much for taking the time to speak to us. I think many of our listeners, particularly, you know, whether you work in the E D or in pre hospital care, anaphylaxis has historically been something that we felt relatively comfortable with, but the more I've certainly read recently, particularly around the emerging mortality data, it feels like the sort of way that we conceptualize anaphylaxis might need a little bit of a rethink.

particularly around the underlying physiology and the treatment principles. And interestingly, my wife has recently undertaken the ePALS or the Emergency Pediatric Advanced Life Support, and anaphylaxis still sits So as someone who is definitely a subject matter expert, I would love to sort of get your feelings on that and ask you a few questions.

around what it is that we need to be thinking with regard to specific subsets of patients. So Ben, if I could firstly just get you to introduce yourself so I don't do you a disservice with all of the different roles that you've got. Yeah. Thanks very much, Rob. I am an emergency physician. I'm a retrieval physician and I am undertaking a PhD in anaphylaxis resuscitation and I'm almost there. It's a slow, painful process, but uh I'm getting there and thanks very much for having me.

Oh, you're more than welcome, more than welcome. And yeah, I take my hat off to you. That's quite an undertaking that you've got there. I know we were just speaking off air before we started around the build up to this. So I mean what is it that you'd like to sort of say with regard to sort of framing the episode? I've got several questions that I'm gonna ask you so I know you're ready for those, but anything you'd like to bring up front and centre?

Yeah, so I think the most important thing for the listeners is to understand that anaphylaxis is a short duration event. The mediators that induce anaphylaxis have very short half lives. The mast cells degranulate and the the whole thing lasts minutes to hours. It very rarely lasts longer than four hours.

So it's a pre hospital and emergency department disease. People who get admitted twice you have a length of stay of less than twenty four hours because they get better before they get there. So this is something that we should own and be experts at. The second thing to say is that most anaphylaxis actually gets better with one or two doses of adrenaline intramuscularly, and sometimes anaphylaxis might even get better by itself because it's mild and it runs its course and it runs that curve.

And the third thing to say is that there's an important subset of people who get very sick from anaphylaxis and people can die. And as you know, my son Max was fifteen and he died from anaphylaxis.

despite paramedic spending half an hour with him while he was conscious and then having uh this process of delayed intubation and that subset is about two to two and a half percent in emergency department settings, but that's the subset that we're really there for because otherwise we'd leave people at home with their epi pens and ask them not to to bother us.

Thanks, Ben. And the obviously the the story about Max, you can hear more about on your website. It's very emotive when you hear you speaking about it. But the the work that you're doing around this to empower us as clinicians and try and bring that subset to the front and center of everything that we're doing is that lap. yn ymwneud â'r hyn sy'n ymwneud â'r hyn sy'n ymwneud â'r hyn sy'n ymwneud â'r hyn sy'n ymwneud â'r hyn sy'n ymwneud â'r hyn.

Yeah, so it's really that uh two to two and a half percent that uh we would call refractory anaphylaxis. So When allergists talk about refractory anaphylaxis, they're talking about people who need more than two doses of intramuscular adrenaline. So that's a subset that hopefully we'll unpack today.

Awesome. I guess if I can start off by framing this a little bit from the outset, I guess at the highest level, so if you're looking at this from the outside, w what do you think from your perspective we've got wrong about anaphylaxis really is probably a reasonable place to start.

Yeah, so I think it's fascinating. A lot of the anaphylaxis guidelines have stemmed from anesthetic practice where hypotension is very, very common, you know, approaching a hundred percent effectively. If you look at the NAP six studies from the UK and

It doesn't necessarily translate to the group that we see in the emergency department and pre hospital, where food is the predominant allergen and insects play a small role and of course there's people with oral drugs But it's a different setting and a different group of patients. So the guidelines haven't evolved to incorporate the emergency pre hospital group of patients that we see. So hypertension is very common in in anesthetic practice.

But actually in emergency departments, uh respiratory symptoms are the most common. If you look at a multi-center study from Australia done by Simon Brown. Wheeze and respiratory symptoms are the most common, and that's in an adult population. And if we look at children, it's less than 10% that are hypotensive. So the emphasis is not quite right if we use your analogy about the ePal's course and having it as a cardiovascular problem. It's more than that.

Yeah, and I think that was one of the things I feel a little bit ashamed by saying it, that I read through your paper and I read through the paper by Tom and his colleagues and I think it came as quite a surprise just to

how I felt like I understood this condition and, you know, had worked around emergency care for nearly twenty five years now. And yet actually, you know, I was predominantly thinking around this idea of circulatory collapse in the vast majority of cases as being the cause. Whereas actually I am

so wrong. If you look at the epidemiology and around the the studies that have been published recently that all right, it might not mean a huge change to the treatments that we're doing, but the perspective you need to have on it needs to be flipped round on its head, doesn't it, around this respiratory component, particularly like you say, if we're in and around a pre hospital or emergency care setting, which is where the most of our listeners do work, rather than anaesthetic practice.

One of the fascinating things about hypertension and anaphylaxis is that it's generally very easy to treat, especially in young people. You need vascular access. you need some vaso pressor, you need some fluids, so adrenaline and fluids, and you just need, you know, twenty two gauge or some sort of cannulary in and y you're ready to go. And it's only when people are really unwell and got multiple comorbidities that that tends not to work. So

Um, if we start with that hypotensive group, the treatment's very well established. It's easy to do, it's not that complicated. Young people with lots of cardiovascular reserve, it's very rare for them to die from the cardiovascular collapse hypotension component.

And you mentioned around the the specific subset of patients, which specific groups is it that we need to be more worried about with regard to this respiratory component? Yeah, so if we look at emergency department presentations, we know that wheeze is very common, but when we look at the relatively rare event of death with anabalaxis The people who die are people who have reactive airways.

asthma or COPD as a comorbidity, where the inflammatory mediators released by anaphylaxis trigger bronchospasm and it can be very fulminant and it can be very rapid. So the group that we're really worried about are people who have coexisting asthma and food allergy. specifically if we just look at that cohort, a hundred percent of people who die from food anaphylaxis die from almost all bronchospasm, with maybe a a small percent that die from upper airway obstruction.

Yeah, the other interesting thing about food anaphylaxis fatalities is that forty percent of them have airway edema coexisting with the bronchospasm. So that has implications for airway management, but the vast majority can be intubated without having to resort to a surgical airway.

Really interesting when you think about how you've historically been taught or from my perspective anyway, I think it might not be the same everywhere in the world. And if we're moving away for this subset of patients from this traditional sort of circulatory collapse, perspective. What's the mental model that we need to have when we're managing these patients that are in extremists?

from listening to your lectures that you've got online on your website, how does that link to the idea of this hard stop being really explicit about the time limits and the escalation? So mental models, time limits, what do you think we need to be having in the front of our minds? Yeah, so I think there's two parts to it. One is to recognise wheeze and shortness of breath as a dangerous symptom and sign and to treat that aggressively because we don't want to end up with respiratory arrest.

So I got an email the other day from some colleagues in Australia who gave a young person who was just uh at the end of primary school. seven doses of intramuscular adrenaline in twenty minutes because she was so cyanized and they were sitting on her about to intubate her for fifteen minutes.

but they were having some trouble with getting infusions going, but they gave multiple doses of intramuscular adrenaline because they knew that they had to treat the bronchospasm aggressively and they got away having this blue child in front of them without intubating her. So

That's a really important take home message that intramuscular adrenaline is benign. You can give multiple doses and that bronchospasm symptoms with anaphylaxis can be refractory to one or two doses. So sometimes you need multiple doses and it's a five minutely drug. So, you know, you've got to be on top of it and uh five minutes goes past pretty quick. That's the the fundamental concept is to recognise it and treat it aggressively.

Because once you turn the corner and you get to a point where symptoms start to stabilize or resolve, then you can back off and you know that you're winning and that you've given the right amount of adrenaline. One of the things that you say on your website is the idea of it being a triage drug, I think is one of the things that you say. And I thought from ID, you know, it's one of those things that you write. It takes minutes to draw up a vial of adrenaline, doesn't it? It takes minutes

It's to get it administered and actually the idea of having an EpiPen sat there next to your paracetamol that you might give out for the sprained ankles and things and empower those nursing staff or whoever it is that's triaging in your department to be able to give that adrenaline as soon as they recognise any problems, you're

You're already several minutes ahead of this case, aren't you, to where you were before? And it's on my audit and quality improvement project list of to-dos, I think it would be fair to say. There's a couple of other things as well that I think that in practical terms, what is it that as clinicians we should be doing differently when we're managing a patient with severe anaphylaxis or asthma related deterioration? So

I'm particularly thinking again about those E D and pre hospital teams. Is there anything that we need to be doing differently or is it just that we need to just reframe it in our mind and act more quickly? Yeah, I think reframing it in our minds and treating it quickly and not being scared to do multiple doses when we haven't turned the corner at five minutes.

You know, if we did that, we would hopefully avoid intubation and deterioration. But what my research into fatal anaphylaxis shows is that once you're hypoxic, from bronchospasm in anaphylaxis. Let's say that's lesson ninety three on oxygen, or you're in respiratory distress, it can be as little as ten minutes before you have that respiratory arrest. And that respiratory arrest will be accompanied by hypoxemic bradycardia, which is our body's reflex to severe hypoxemia eventually.

But what we need to do is know that it might happen in as little as ten minutes if someone's hypoxic or in respiratory distress. So that means getting somebody to get equipment and more drugs and more adrenaline ready to go. So it can unfold very quickly. It can be the most challenging thing to do.

The next thing to say is that once you have that hypoxemic bradycardia, that's the brain and body's way of saying, I'm checking out. It's this reflex that evolved probably when we were fishes in little ponds and we ran out of oxygen. to try and survive. But in humans that bradycardia really is associated with brain injury. So you've got four to six minutes before there's brain injury and it's a hard stop as to

saying that the cure for that hypoxemic predicate is oxygen. Yes, we're gonna give adrenaline. And for example, when my Max died, he had

you know, three rounds of adrenaline and C PR with a bag mass ventilation. That didn't help him. It was once he was intubated and had oxygen delivered under those conditions where he needed high peak pressures to overcome the resistance with these Bronchospastic lungs, it was the intubation and delivering oxygen under pressure that made his heartbeat return and his blood pressure was normal very, very quickly.

But uh the hypoxic brain injury ensued. And so that's really the key. Once you have that hypoxymic bradycardi, the oxygenation is the absolute priority. And there's obviously different ways of doing that.

I think that sort of leads us on a little bit to I guess I work predominantly in an E D setting where we have the option to provide drug assisted intubation or intubation whenever the patient requires it is the summary but For a proportion of our listeners, they won't have either the option to do drug assisted intubation or won't have the option to do intubation per se, as in we've moved quite heavily towards superglottic airways or cardiac arrest management in various places around the UK.

In terms of those clinicians that are out there, what is it that they can do in that extremist situation or what are their priorities going to need to be, I guess? Yeah, so I think one of the absolute indications fendotricheal injupation is bronchospasm. So we know that bag valve mask and laryngeal mask will be ineffective at some point.

But it's not impossible at the beginning and we all reach for the bag valve mask to begin with, don't we? And so when Max was a few minutes out of hospital, he became unconscious and was briefly bradycardic. But it was the bag valve mask from the paramedics that oxygenated him and resolved his bradycardia and he'd then for the next twenty minutes

had a normal heart rate and a normal blood pressure and and was able to be oxygenated. So bag valve mask can be a temporizing measure and it's probably gonna inflate the stomach a little bit. There might be a risk of aspiration. So, you know, just using suction as you need, being aware that the chest is gonna feel like a brick bag, you know, you're gonna get that feeling of very high resistance. But that you should absolutely attempt to oxygenate because that's uh that that that's the key.

I got another email or contact from another family whose child recently died from anaphylaxis where the paramedic crew just used an LMA. And I think, you know, depending on how the LMA sits, depending on what sort of seal you can get with a bag mask, you know, obviously one might or may not be better than the other.

But just really if you're not getting a seal with the LMA or you're feeling like you're just getting leak, then try at the mask instead. There's no right or wrong answer. But it's a temporising thing and you just need to give the heads up to the place where you're going to say, we need a tube on arrival, which is a really important part of what paramedics do is giving that notification to say what's required as the next step.

Yeah, absolutely. And you know, that phone call, that pre alert describing exactly what it is that you need in terms of response when they arrive is absolutely critical, ensuring there's no delays at the following end and being clear and concise with that, I think it's amazing. Is there anything from a pre hospital perspective we can do to

predict those patients that will deteriorate like that? You've already mentioned the subgroups, I guess, with regard to the food and the background history of asthma or C O P D. Is there anything beyond that you can use to predict? Uh, it's really hard. It's one of the most difficult things about anaphylaxis, and this goes for the E D people at Triage as well, is that nobody can predict.

when a reaction starts, how severe that's gonna be. So we haven't worked that out. We're trying to develop registries where we can try and look at variables which might help identify those people who to be okay and those people who are at higher risk. But at this very point in time we don't have enough data to say who's going to deteriorate and be in cardiac arrest in fifteen minutes and who's going to be absolutely fine after one dose of adrenaline. It's bizarre.

It's a really unusual disease in that respect, but you know, bearing in mind that ninety eight percent will do fine and that's why we're lulled into this false sense of security. So that's one of the take home messages is just You know, if things are better, that's great. You know, treat hypertension on its merits. Uh everyone's pretty good at that. But uh if they're weasy, just treat it with respect'cause it can evolve pretty quickly.

Oh, that's amazing. Look, Ben, thank you so much for your time today and thank you so much for sharing your expertise and sharing obviously the story that you've got personally and Max. We'll make sure that everyone gets directed over to that website where you've got some amazing resources and clearly we'll uh

keep abreast of all of the publications you'll have coming out with your PhD because it's gonna inform us massively and I think, you know, our listeners will find this hugely useful. So thank you so much for your time. I do really appreciate it. Good luck to everyone. I hope everyone has a great shift next time they're working clinically and thanks for having me.

Yeah, well a huge thanks to Ben for giving us his time and his expertise with that interview. I mean, we said it beforehand, it is an unbelievably powerful piece of work and and what a legacy to give to Matt.

He also mentioned in the interview about the resources, the fantastic resources that he's developed out there, and in that was the Amax four. So Rob, come on, tell us a bit more about that. Yeah, so on the website you can find it's the Amax four algorithm. Everything on there is free and open access. There's lectures. I

I'd thoroughly encourage you to go and watch all of them. I think there's four and then there's a particularly one titled Just a Routine Resuscitation which is really worth a few minutes of your time. But A Max four is essentially the algorithm that you should be considering for these patients if you ever get encounter this situation. So A stands for adrenaline, M sounds for muscle relaxation, A

stands for airway with a cuffed endrocheal tube. X is extreme oxygenation and obstructive ventilation strategy. And then for four, so that's aiming to achieve that definitive oxygenation within four minutes. to avoid that hypoxic brain injury. Now clearly There's a lot more detail there as in how much adrenaline. Well, go and take a look because there is a really useful aid memoir that you can download and keep with you and it's got all that information there and it is far better to digest.

uh in your hand than it is via your ears, put it that way. Yeah, and what you mean by that, Rob, is that he actually explains it much better on the website than you can. But um that is absolutely fair enough. Slightly cutting, but I agree. Yeah, and Amax four, just to give that bit more context, that is essentially a best

practice algorithm for critical care clinicians in anaphylaxis and asthma resuscitation. So I guess in my mind the place for that is in that refractory anaphylaxis, but in these really time critical situations, if you go back back to those times that Rob was talking about earlier, fourteen minutes average time to be in absolute crisis in arrest for some of these cases and and I'm sure quicker in others

You know, this is something that we need to have absolutely drilled in our minds. We want to be making sure that we're treating anaphylaxis. quick enough by recognizing it early enough that we don't get to this position. But if we were to get to that position, then A Max four is something that we need to keep in our mind.

Yeah, I mean I think there's a couple of things also from the interview which was phenomenal and it was great to get so much of Ben's time and I think one of the things that surprised me so much from it was just how much my interpretation of anaphylaxis

uh presentation and management, i.e. cardiovascular collapse, had been influenced by the anesthetic literature and I didn't know that at all and the influence of things like NAPSIX has been absolutely incredible, hasn't it? I mean what was your take on that, Langus? Yeah, well I think NAPSIX is a fantastic piece of work, but what we're looking at there is patients with perioperative anaphylaxis and therefore we're potentially looking at patients that are intubated and ventilated.

And therefore those subtle respiratory signs that Ben was mentioning in the interview, we're not gonna see those in those presentations. That's not the same as a conscious patient that's spontaneously ventilating. So that isn't berating Knapsics' work, but we've just got to remember, just like with any evidence that we look at or any database, that it's specific to the context within which it's being studied.

That's it. The generalisability, isn't it? It's the generalisability of those findings into the E D and pre hospital setting, you know? Yeah, absolutely. And you know, you picked the title of Reframing Anaphylaxis and I thought it was a bit of a bad choice at first, but actually this is all about that, isn't it? Because

We're not really challenging the guidelines or challenging the evidence. We're challenging the way that we do have it framed in our mind and when that triggers for the differential being anaphylaxis when we're seeing patients.

Oh yeah, I mean for sure. I think that's a that's a really nice summary of it actually. I Yeah I mean there's one other bit and th this is again, you know, if you're if you're involved heavily in critical care all the time and you do it as part of your day to day life, it's almost second nature, you know, around things like ventilation strategies in that

severe obstructive physiology. But I mean, for someone who isn't, or for the people that aren't doing that day in, day out langers, what does that actually mean? As in, what does that practically mean out there in practice? That ventilation strategy. Yeah, so that's again there's fantastic resources on that website to go and have a look at.

This is looking at a ventilation strategy for these groups of patients, for that mixed anaphylaxis and asthmatic population, that we're going to be looking to try and deliver oxygen as the absolute priority, and we might be compromising our CO two targets a bit in doing that. So we're going to be looking at things like small tidal volumes, longer expiratory times for that gas trapping, accepting high airway pressures.

accepting the risk that we you know, we obviously don't aim for that in our standardly ventilated patient, but this is absolutely extremists trying to avoid that dynamic hyperinflation. And obviously trying to watch out with the risks in delivering ventilation like that. in these patients having a pneumothorax. So yeah, fairly similar to the way that we're going to be looking for our standard asthmatic, critically unwell asthmatic that's intubated and ventilated.

Yes, indeed. Awesome stuff. Loads to take away and think about, even though it's not really new stuff, it's just like you say the reframing of it and that new information that's come from those new data sets. But I mean it feels like a good time to wrap up, Simon. Dunno what you think? Yeah, we haven't got James dragging it out anymore, so yeah, let's tie it up at this point.

Excellent. Well, a huge thanks to Ben for coming on the podcast and sharing his really personal story and the amazing legacy and work that he's done. Following Max's tragic death. It is definitely worth going over and having a look at the website, which we'll hyperlink to, which has got some fantastic educational resources on this.

I think in the process of prepping for this and listening to that interview, there are a few bits to take away. So, in terms of anaphylaxis, we know it can be difficult to pick up, we know the definitions can be difficult to interpret. Spending the time to think about it and thinking about the triggers of when you're going to go through the treatment algorithm that you'll find in those great guidelines is really time well spent. We shouldn't be relying on the rash.

Airway and breathing deserve real respect. We're not gonna be waiting for that circulatory collapse to Treatment. And I think really importantly, don't be fearful of the adrenaline. Now, also remember to take a look at the RCU.

document in terms of biphasic reactions. So five percent of patients are gonna have biphasic reactions. That's gonna influence the time of observation in the emergency department and influence how you're going to safety net and who might be appropriate to be discharged at which point. that is slightly nuanced depending on those different features that are patient centered.

And also, as we mentioned, we want to try and ensure that we treat anaphylaxis really effectively and have good outcomes. But ultimately, a lot of this is about preventing another anaphylactic reaction, which means we need to get a diagnosis. I think we need to be really conscious of the fact that that is an important part of our ED management. Think about those mast cell triptases. Think about the time within which.

taken in your emergency department and try and benefit that patient for the next That they might have. A huge thanks to Zol Medical Corporation for collaborating with us on the podcast, for making this all free, open access, and available to you. And we will be back. With another Papers of the Month and Roadside to Recess when we get all of the band back together for you next month. As if we would ever make it into a band. Right, so take care of yourselves and we'll speak to you soon. Speak.