IBCC Episode 77 - Anaphylaxis

Alright, so welcome back to the Internet Book of Critical Care podcast, I'm here with Adam Thomas, and we're going to talk about anaphyl access. You can't resuscitate if you don't know how to cover this right away because you don't have a lot of time when the patient's crashing in front of you. So today, this is going to be a relatively quick podcast because there's not a huge topic to cover here, but we need to know the basics very, very well. So the kitchen sink and then all the sick wildlife that you can have. This gets straight into a Josh clinical findings and clinical definition of anaphylaxis because I think a lot of the time is people aren't thinking that this is anaphylaxis, they don't appropriately address it, and of course, epinephrine, not giving it if you don't think it's anaphylaxis, increases mortality. So let's cover it to be sure. Anaphylaxis can involve multiple different organs, and this can be tricky because it's not going to always involve the same exact pattern of organs and the same constellation. But the key ones are probably number one, at least in my mind, would be the skin and the mucous membranes. This is going to be seen in about 80 or 90% of patients. You can have flushing or to carrier itchiness, antiodema, conjunctivitis, stuff like that. Then other major organ systems involved, cardiovascular, certainly we can have cardiovascular collapse, hypotension, shock, syncopy, death, pulmonary involvement. This can be the upper airway strider and also the lower airway with bronchospatum patients can have dysmi and cough. And finally, GI manifestations, nausea, vomiting, abdominal discomfort, diarrhea. I'm going to skip forward to the definition and then we're going to come back to chronicity because I think they build on each other. So remember, the approach to the diagnosis, it's a clinical diagnosis. You're not going to wait for the differential and the mass cell and eosinophils to come back. You need to diagnose this on the spot. So the three hallmarks are exposure history and the timing around exposure to symptoms, the number of organ systems involved. And is this likely the diagnosis or is something else going on? So are there competing diagnoses? So Josh, walk me through the exposure and the cronicity. There's this really complicated diagnosis out there in the universe and I think it was like put together by our guests and it just confuses me a little bit. So we've broken this down and simplified it a little bit. So as far as exposure history and cronicity, this can certainly support the diagnosis. So if the patient was stung by a B or exposed to some sort of hour chain or some sort of medication, then this could definitely bolster diagnosis of anaphylaxis. That being said, there are patients who have idiopathic anaphylaxis. So the lack of a trigger certainly doesn't exclude anaphylaxis at all. And the timing you broke down here specifically in the post that depending on the exposure and the antigen type and take it with a grain of salt, usually the time course because of that. So say if I give Iatrogenic anaphylaxis, say contrast mediation, if you want to be controversial or a medicine, and they're immediately allergic to this, what's the onset of anaphylaxis to death with Iatrogenic anaphylaxis? So the average time from giving an IV medication to death in one study was five minutes, which is shockingly fast. And that's going to kind of tend to be biased toward more severe reactions. So I'm not saying everyone has reaction within five minutes, but it's going to be really, really quick if you're giving something intravenously. Alternatively, if you get a bee sting, that's typically going to cause anaphylaxis within about 15 minutes. And food anaphylaxis may take a couple hours, but typically this is going to be within pretty tight credicity of whatever stimulated it. Exposure history. They don't need it, but likely they have an exposure. So food or some other antigen flying hemianoptera and venomation. Take your pick. The next up, number of organ systems involved. This is pretty straightforward. Two organ systems strongly suggest the diagnosis. So I have angiademia and I have abdominal pain. I have erdecaria and I have dyspnea. Those kind of things. Two systems anaphylaxis. Anything else you want to say about this, Josh? You can also have anaphylaxis with one organ system in a highly suggestive scenario. So if someone was tongue by bee and they came in and they have history of anaphylaxis and blood pressure of 60, that's a page with anaphylaxis, even if it's just one system. At least I would treat them for it. I think another theme here too is when in doubt, I think you're probably better off airing on the side of treatment. I completely agree and it really depends on what that system is involved and the acuity. So they get stung by bee and they're hypotensive. That's just cardiovascular, but that's a threat to life. Or they eat some peanut butter and they have angiademia. You're going to treat all those things like anaphylaxis. Exactly. Let's throw a wrench in this whole thing though, Josh. And say, what if you think there's something else going on? Should you pump the brakes and not give them the kitchen sink approach that will cover? Like everything in the IVCC, this all depends on clinical context. But I think in general when in doubt, if you're treating a sick patient and you think that they may have anaphylaxis, you're going to probably be better airing on the side of treatment. So we'll talk about the treatment in a little bit. But put them on some IV epinephrine infusion, give them some steroids, give them some anti-histamines. And I've certainly had patients where I've done that and allow the dust to settle if you're wrong and you could put the patient on an epinephrine infusion for an hour or two when you're monitoring them. And they're going to be totally fine. But if you fail to treat, then that could be really bad. You're speaking to my merch ways, Josh. For what is that? For what is that? And diagnosed at the same time. It's the ICU wave edge. Just do everything. Stereoids, epinephrine. Antibiotics. Antibiotics. Antihistobites. Let's do it. So let's remind everybody of the causes here. Pretty straightforward. This not an exhaustive list. So foods. Big, big ones. Peanuts, seafood. And remember, with seafood, it can be a primary allergy or you can get some scombrid in there. We go into that insects flying hemianopera. So bees, wasps, those kind of things. Medications, especially antibiotics. Don't get Josh. I'll fire it up with the penicillin in first-generation cephalosporins and cross-reactivity. My favorite the other day, Josh, about to give Peptizo. Don't give me that. My mom's allergic to it. Favorite allergy. Inceds, aspirins. Monoclonal antibodies. Be especially worried about anti-TNF antibodies. Radial contrast die. Again, a complex topic, but it's out there. Parallelidics. Prodamine. Local anesthetics like lidocaine, benzachine, and mipivite gain. Blood products. And especially if they're IgA deficient. And then cool, exercise, cold or heat exposures can do it. Josh, not exhaustive, but let's move on. Investigations. Is there a laboratory investigation to confirm anaphylaxis? Or what tests are unicent? This is kind of fastening in modern medicine. So there's no EKG. There's no CAT scan. There's no MRI. There's no lab tests. There's no test that's going to basically tell you whether or not the patient's having anaphylaxis in real time. If you want to send off a triptace level, that may come back next week. And that could help the patient's outpatients, you know, allergy specialist. No, whether or not they had anaphylaxis. So if you want to do that, when the dust settles, great. Go for it. But there's no test for this. This is really a clinical diagnosis. And it's just a matter of getting a good history, good physical, considering your differential. And then the tests that you do are really going to be aimed at evaluating for alternative diagnoses. So, you know, oftentimes these patients will present and it may be anaphylaxis versus sepsis or anaphylaxis versus pretty kind of mediated angiodema or anaphylaxis versus PE. So you may need to do some evaluation to look for the other things going on. But there's no test for anaphylaxis. Moving on to diagnosis and differential diagnosis. So this is important to work in the back of your mind. Like we said, you're going to start your treatment upfront when they're this second front of you, but you're always going to go for the hunt for the right October. So asthma, severe asthma is a risk factor in itself for anaphylaxis, but they present the same as well. Wee's dysmia in an asthmatic patient can be just bronchoconstriction from the primary pulmonary disease or a stigmata of the underlying anaphylactic response. Angiodema due to bradokine and accumulation. We've already covered this. Check out that podcast for more systemic mastocytosis. Awesome to bust out during rounds. Very difficult to ascertain in the seconds that someone's crashing in front of you. Add a phallac toyed reactions like red person syndrome due to vancomycin or scromboride like histamine fish, all your dark meat fish like tuna, upper airway obstruction of any ideology. So paradoxical core dysfunction, apocotitis, some abscess, can press in your airway. The last two. Cupid pulmonary deterioration, like think about your PEs, pneumothorax, other obstructive shocks, and the grand mimickers of toxic shocks syndrome the extreme or sepsis in general. Josh, let's bring back an old friend, kicking an old school with a podcast we covered a while ago. The big thing that we're always trying to figure out is this a histamine mediated process or a bradokine and mediated process? How do you walk that out and how do you treat it? For patients who are manifesting with a predominantly angiodema type of presentation, the question is always going to be, is this histamine mediated essentially anaphylaxis or is it bradokine and mediated angiodema? And that's more of like the ACE inhibitor-arb type thing. But we had a separate cast on that. And there's a table here that kind of sorts these things out a little bit. Your histamine mediated anaphylaxis is going to be faster. There's going to be more diffuse distribution of findings and the skin and other parts of the body. And these patients are going to respond better to things like epinephrine steroids antihistamines. So sometimes based on the history, you can get a pretty good concept of what's going on. So if you feel confident about the history, for example, someone has like the classic asymmetric tongue and they're on ACE inhibitor, you could probably feel pretty good about that, especially if no other features of anaphylaxis. Alternatively, if they have like multi-system hematidamic collapse, they're clearly that side of anaphylaxis. So if you can sort it out for sure, then treat it. If you're not sure, I think the best thing to do is to give the patient a round of therapy for anaphylaxis. And if they get better, then they probably have anaphylaxis. And if they're really refractory to therapy, then they may actually have a brady kind of mediated process. Great summary. Check out the post for more. If you guys look at the specifics and of course reviewing the ideology, you're going to treat for both upfront if you have a sneaking suspicion. Move it on to source control. Josh, if the antigen's present, it's going to be hard to keep cranking the epinephrine and stop the response. So what's your approach to source control? Certainly, if you could call to the bedside and someone's potentially having anaphylaxis, we actually want to stop any medications that they're on, you want to stop any blood transfusions that they're on. There is this concept that if someone has like a bee sting or just got like subcube, lidocaine or something, you could put a tourniquet on that extremity and just prevent further medication from coming into the body of never done that, but it sounds kind of interesting. I'm going to try that next time. All right, let's move to the homework. When there is mortality and benefit in anaphylaxis and we're going to be very clear about this, Despite everything we do, you only chew mortality benefit epinephrine. So it's important to give epinephrine if you think there's anaphylaxis. When people run into trouble, because they don't use epinephrine when there's anaphylaxis. So Josh, starting with the basics, of course, airway breathing circulation, tell me about why this drug is so important. I actually didn't realize this for a long time. So for a while, I always thought like, you give epinephrine to patients who are hypotensive, right? It's like a presser drug. It's a positive antitrop. It's a positive crototrop. But epinephrine actually does a lot of other really good things in anaphylaxis. So it stabilizes mass cells and that prevents this ongoing cascade of mediator release. It can reduce airway edema. It can dilate the bronchules. So basically does all of these different things. They can actually help stop the underlying process of anaphylaxis. So even if the patient is not hypotensive, giving them epinephrine may stop anaphylaxis in its tracks and prevent them from getting sicker. So essentially, anyone who we really think has anaphylaxis should get anaphylaxis. I totally agree, and it's so much fun for someone like me who's not a smart guy, that airway, airway problem in anaphylaxis, epinephrine's answer, breathing, breathing difficulty, epinephrine's answer, circulation, hypotension, epinephrine's the answer. So it is very straightforward. So just pull the trigger early. And by the way, I should credit Ruben Strayer for that ABC algorithm. He presents that in MRI. So basically, indications, Adam just said ABC or if you have two organ systems, those would all be reasons to give epinephrine. Ruben gets credit for a lot of things, very, very smart clinician. So let's talk about how to give it. Traditionally, we're all taught I am epinephrine, and if you give it any other way, you're wrong, gosh. 0.3 to 0.5 milligrams, that's the EpiPen dose, that's where they get it, mid anterior lateral thigh, maybe the shoulder if you're getting crazy, and if they get any other symptoms again, bam, we hit them with another dose. Maybe three, maybe four EpiPens in them, right? That is a completely legitimate and appropriate therapy for antiflexus. And I don't want people to come away from this podcast saying that I don't think intramuscular epinephrine is a good thing. I think it's a great thing, and especially in the pre-hospital arena, or for folks who have epiPens, or if that's like the closest thing that you have, and you know how to use it, go for it. But I have to say that from my kind of skewed vision of this in the ICU, it's actually quicker and easier for me to get IV epinephrine in the ICU, I've never actually used intramuscular epi in the ICU, because we just have IV epi all over the place. So my preference would actually be to use intramuscular epi, and there are a bunch of potential advantages to this. So first of all, it's faster on set. So we said earlier that if someone gets an IV drug and it kills them by antiflexus, they often will die in five minutes. So if you give someone I am intramuscular epinephrine, it takes several minutes for it to get from the muscle to the blood tissue, especially if they're in shock that can take a while. Whereas if you're mainlining the patient, if you're giving them IV epinephrine, it's going to go faster. Obviously I'm assuming that the patient has pre-existing IV access. It's easier to taper so you can kind of start it, you can stop it, you can titrate it, and you can also withdraw it if you want. So for example, if you give someone a big slug of intramuscular epi and their blood pressure shoots super high and they start having angina, you can't take that away. You've given them that epi, they're going to have that epi on board for like 15 or 20 minutes. Whereas if you give them IV epinephrine and blood pressure goes to how you can stop it. So there are never reasons that I kind of prefer this. I totally agree, especially the emerged population very different than say our code population when we're getting called. I think the classic example is someone down getting their cardiac CT, which was wrought with its own problems, they get their contrast, they have a contrast reaction, and they just got plugged with maybe one or two generous doses of epinephrine. And now you've traded one problem for another because their blood pressure is 260 in a heart that's getting worked up for the Schema Cardiomyopathy. So again, like you said, I don't want people to come away with this. The safest thing if there's antiflexus is always to give epinephrine. And if I am epinephrine is the only thing you have access to go for it because it's much better have a little too much blood pressure and we'll have to work that out than to have no blood pressure and they arrest on you. So that being said, I do like the IV epinephrine because I agree our code teams are ICU, nurses are very familiar with it, everybody knows how to titrate it and how to do it. But let's talk about maybe the populations that listen to podcasts that don't use regular epinephrine infusions. Tell me about this dirty epi drip that kind of emerge and full med community are super into. If you don't have a pre-mixed bag of epinephrine on hand, what you can do is you can take a milligram of epinephrine and that's either going to be the syringe of cardiac epinephrine that tends to be syringe or you could use the one milligram of one to a thousand intramuscular epinephrine. Basically either one of those will have one milligram of epinephrine and you're going to shoot that into a one liter bag of lactated drinkers or typically normal saline, shake it up. You can create a one microgram per ml solution of epinephrine and I really like this for several reasons. First of all, it's easy to create and you can kind of get it anywhere. The literature is kind of terrified of people overdosing on epinephrine and there's this whole fear that we're going to give people too much epinephrine and their hearts going to explode. Once you dilute your epinephrine into a one mic per ml solution, it's basically impossible to overdose your patient on it. So even if you squeeze that liter bag wide open, you're basically going to be giving your patient probably a max of like 30 or 40 micrograms per minute of epinephrine. So it's not going to be enough epinephrine to kill them. So once you've taken the vial of cardiac epine and squirted it into the bag of saline, you basically created a situation where you're not going to, it's really unlikely that you're going to overdose the patient on epinephrine. And 30 to 40 is a moderate dose. It's not even that much epinephrine. If you look at refractory vaso-plegic shock, so totally safe to do, reach out out because I think Brian Hayes, that's the first person I heard it from academic life in emergency medicine. And I've used this, it's easy to do on the cold card, especially in a merger ICU, it's really hard to get that epinephrine infusion from somebody who doesn't use it all the time. So the dirty epi is super easy to make because you got the cold card epi, squirt that in a liter and start wide open. I've just quickly just touched on the actual dosing of the epi. There's not super solid evidence on this, but I think a reasonable approach is if the patient is dying and they have no blood pressure and they're like about to die, you probably want to give them boluses of like 20 to 50 micrograms of ib-epi, a pushdose epi. Once you're kind of past that, or if the patient is not peri-rest, then I think you could probably start them on like 20 mics per minute for a couple minutes, but then you're going to want to drop them down to about 10 mics per minute as it maintenance dose. And I think probably a reasonable target for most of these patients initially is 5 to 15 mics per minute. And then one other challenge of the epi drip, and honestly, I think the biggest problem with the epi drip is that people are afraid to wean it off. So it comes in with anaphylaxis, they get the epi drip, they respond fantastically, and then there's just this like fear that like you can't stop it and it'll just stay on forever. Yeah, that's the same fear people have for a lot of interventions we do in medicine and it's easy to turn it off and turn it right back on, like you said, because it'll work right away. And the other thing I'd the caveat I want to say for potential haters out there is remember we're giving 500 micrograms I am, and you can argue whether you don't know if it's I am or not, and the pharma kinetics and dynamics, et cetera, et cetera. About 500 mics, 50 mics, order magnitude different, I think the loading dose strategy here is very smart to go. Yeah, you know, admittedly the evidence basis here is low, and this is one of these critical care things where like no one is ever going to do a good study on it. And the retrospective studies show that people who get ibup do worse because they're like the sickest patients. So I think overall I think this is a reasonable thing as long as it's done by folks who kind of understand how to do it. So let's move on to the cocktail treatment, which I call the kitchen sink and you throw everything at these patients because it's really important to get treated right away and play the short and the long game, meaning the immediate effective doses and then what's going to work for long term inflammation. Let's break this down, Josh, like you have into the non beta blocked patient and the beta blocked patient. So up front, non beta blocked, what's your kitchen sink slash the pharcus cocktail? Yeah, so we talked about epinephrine, so that's the most important thing. And honestly, it's probably more important than any of the rest of the stuff, but assuming the patient's already been on that, the next thing is steroid. So steroid is not going to bail out your patient within the next couple hours, but it makes stabilized mass cells and may prevent further deterioration over several several hours. And so basically going to get steroid, who knows exactly how much I think giving them like 125 of methyl prednis loans, reasonable. And then you could probably taper it off pretty quickly. And then we get to our dual antihistamine blockade. So something like an H1 blocker, such as diphen hydramine, 50 milligram, and an H2 blocker, such as famodity and organidity. And that's basically the cocktail that I'm going to give most of the patients. So epinephrine steroid, H1, H2, and then you can throw in some inhaled up uterol on top of that. If patients have, I'm going for acroisephasia. Although deep in my heart of heart, I've always wondered if they have persists in bronchospasm, should I be using the epi to treat the bronchospasm? I don't know exactly, but just make sure that you're not purely using out buterol in no epi-defer. To be honest, I'm a bit of an inhaled epi guy, and I have the epi at the same time. Nice. All the, I just drawn them in epi. All of the epi. Let's talk about the thing I need to remember all the time, are they beta blocked? So the six-year-old male comes in hypotensive, just ate something he should love, and now I'm treating them anaphylaxis, but it's weird, Josh, because despite him being so sick, his heart rate doesn't budge about 70. Oops, I checked the mar, and he's got this opera law at home. So how do I approach him? I'm going to use the kitchen sink, but what else am I going to give him to make sure my epi is working effectively? So I think the first point here is that I think most beta blocked patients, and I'm going to make this statement with no evidence basis, and who knows if it's right or not. But my guess is that most beta blocked patients would be totally fine with a standard therapy for anaphylaxis, and my guess is that for the vast majority of patients, the epinephrine could overcome their 25 or 50 or 75 milligrams of a total of all. I wouldn't get like two off-put by the beta blockade. I think if you kind of use your standard algorithm, you'll probably be fine, but you may definitely encounter patients who are not responding to therapy. So when that happens, what can we pull out? Glucogan seems to be the standard recommendation here, and the concept is similar to beta blocker poisoning. It can kind of like sneak past the beta blocker. beta agnostic receptor and increased intracellular. or cyclic ampere level. So you could give these patients IV Cucacone. I'm not a huge fan of this. It makes everyone puke, but I don't know. - You know like puke Cucacone? (laughing) - I don't know. I feel like unstable patients with wonky airways, but like that's not super great. - I can't breathe. Would you just give me, ah! (laughing) (laughing) It's the best. What about meal renown? You ever sneak that in there? Theoretically, I think meal renown could be something that you could use. I might be worried that it would cause peripheral basal dilation, but if you have a bunch of epion board, that would probably be okay. So I think meal renown would be another consideration if you had someone who really had straight up refractory shock. And isoprotonal would be something else you could use to just try to like completely overpower the beta receptor. But another thing too, and we'll get to this just in the next section, is always just go back and take a look the patient's heart to an ultrasound, because it may not be the 50 milligrams of hematoprol, and maybe they have no intravascular volume, and maybe they just need volume. So I don't know, don't get too hung up on the beta blockade thing necessarily. - And I will just put this out there here, 'cause I've come burned out this, 'cause playing with isoprotonal millenon, very interesting. But refractory shock in the case who I thought was anaphylaxis, who was, turns out it was also a medication error, and got too much epi, and not until when we looked at the heart, and saw an 18 year old heart that had an EF of like 5%, to be realized something else was going on. So it's important to step back and always assess your shock patient with a basic approach, and don't be stuck on the usual stuff. Let's move on. You said the groundwork fluid resuscitation, Josh. I feel like you got Alzheimer's, or you've been listening to Trump feel much, 'cause you are advocating for fluids. - Yes. - It's wrong with my dear, dear friend, Josh Farcus, and who are you? - I think this is actually probably one situation where large volume resuscitation may be reasonable. These patients can drive, say, a lot of fluid, and cardiovascular collapse is one of the causes of death here. So if you think about, I don't know, from a nice used standpoint, we're always thinking about, "How are these people going to die? "What do we need to really worry about?" And they're going to die from loss of airway, or from cardiovascular collapse. And anyway, loss will talk about in a second, but I think when they first roll in, and they're really kind of sick, I think throwing a fair amount to fluid them is probably a reasonable thing. I kind of like the flip side here is that ideally, these patients are going to get a lot better within the first couple hours. So they're going to hopefully mobilize that fluid quickly. So this isn't going to be like a sepsis thing where you dump six liters in them, and then like the next day, you put another five in, and hopefully it'll be something where you give 'em, three or four liters, you throw the kitchen sink at them, two hours later, they're a lot better, and then before you know it, they're like a lot of die-reasing in there out of the ICU. - I totally agree, 'cause as you said, timelines, even if it's between five and 30 minutes, they're gonna die in front of you if you don't intervene right now, you gotta play the short game and at the detriment, maybe to the long game. So that's the groundwork for airway management as you alluded to. So they're either gonna die because they're pump and their pipes are so empty. So cardio vascular collapse, or airway gets obstructed. So talk to me about the major hallmarks here, of course, epinephrine, but other approaches to bronchodilation, airway securement, and why I can run into trouble. - Initial things you can do to temporize the patient, so if you have an anaphylaxis patient, and they start having a little bit of strider, or we think the main needs to insubate them, but need a little bit of time to get all the material, get the right people ready. So heliox can be a good stopgap measure here to kind of allow patients to breathe through that, constrict it up her airway, and nebulized recemic epinephrine may also improve things a little bit. These are not definitive therapies, so I'm not saying you should like put your patient on heliox and nebulized recemic epine, walk away and forget about it, but this could buy you an extra five or 10 minutes to get everything ready and kind of do like a slow, methodical intubation. - And I find it's always one of those things we say on our exams and in the textbooks, but logistically trying to get a heliox into the drama bay or at your code is never happens, but yes, it's on the list. (upbeat music) - So traditional indications for intubation, then I think we know these, but sometimes they can lead us astray, can't they? - Yeah, I mean, this is tough. Honestly, this is really like a black box of evidence. These cases can evolve really rapidly. I think one difference between anaphylaxis in bradykina angiodema is bradykina angiodema tends to move a lot more slowly. So there's more time to, you know, do an nasal angoscopy and like reevaluate the patient anaphylaxis moves pretty quickly. So I think that can really make it difficult to know exactly what the indications are to intubate the patient. Honestly, I'm not going to pretend that I have like a perfect list of criteria. I think a lot of this is a clinical judgment based on how bad the patient is, what direction they're moving in, stuff like that. - I wholeheartedly agree. It's really hard to give you a recipe for this 'cause it is very patient specific and also interplays with our own individual risk tolerance. So that being said, we are going to approach this airway in the effort to secure it. When can I run into trouble? - Yeah, so this is a true airway disaster. So first of all, you have anatomic problems. So the airway may be swollen. You may not be able to see anything. Minipulation could make things worse. Position could make things, the patient may be stuck in one position. It's kind of like keeping things open. And then when you go to lay them back, you could potentially obstruct the airway. So we have all those anatomic problems, but then you also have the cardiovascular problem that these patients may be at risk for human-dynamic collapse. So this is really just like a multi-dimensional airway disaster. - Favorite case ever? - Okay, so let's break it down. Tell me how you're going to approach two general scenarios. A crashing anaphylaxis patient, which is rare or the non-crushing anaphylaxis patient. - I've kind of outlined two schema here in, I don't know, take it or leave it, see what you think about it. But there may be some patients where they're strigilists, they're really about to obstruct the airway. They're on the verge of death. And one problem with these airways is especially if they're lips and they're tongue are super enlarged, that it may be impossible to intimate these patients from up top. And if you paralyze them, you could run into a lot of trouble. So I feel like if a patient was truly about to die and about to lose the airway and looked on the brink of death, there could potentially be a place here for giving the patient a dissociating dose of ketamine and just doing like an awake dissociated crickery, just cut open the crickoid membrane and put it in an airway. - Agreed, if you think access from above and is impossible, that's the way to go. And of course, if you always have time, get all your friends around to help you with a double set up. - Exactly. And that would be the much more common scenario, which is patient isn't doing well, but they don't necessarily need like media and airway management. So in that situation, we do the double set up where ideally you do get an awake fiber optic indication from up top, but then you'd have a friend ready to do a cragothertomy at the same time if you encounter problems. - And I think the biggest thing we've talked about on a lot of posts and I think a lot of people online get the point about it is, Laura, down again, it pushes, it's just make that decision and go early and it doesn't matter if it's a surgeon or not. They just need to make sure they know the procedure well and they can do it in a timely manner. - Absolutely, absolutely. (upbeat music) Let's talk about recovery. You alluded to this before. Everyone's afraid of stopping the epinephrine and how long do I have to wait for the steroids to kick in. - Once they've been on epi for a couple of hours, things are getting better. You probably just wanna wean it off and just follow them carefully. And if they get worse, you can put it back on. I honestly, I think the real drawback to epi is just leaving it on forever because that's when your cumulative epi exposure really is going to increase. As far as steroids go, I don't know. There's some purists out there who kind of say that there's no good evidence for this and you shouldn't even use steroids at all. I think most of these patients realistically are going to get a course of steroids, but I think it can be like a three or two day burst of steroids. I don't think we need like a lot of steroids. - I totally agree. - In general, vast majority of anaphylaxis patients are seen by primary care and emergency physicians in an urgent care/emerge perspective. They settle down after one round in epi, continue some remnant eating and some diphon hydramine soy. And then they don't need maybe one dose of steroids, but what we're talking about in this post is ICU level anaphylaxis. You're on an epi-infusion and I agree, even though the evidence doesn't point to there. Anyone who's getting that much epinephrine is gonna go home one, two to three days of steroids so that I can sleep well. And maybe I'm wrong about that, but we'll allude to it in disposition, but my basic reactions while they're low, I think the antigen exposure and response are very different in the population we're talking about right now. But before we do that, how about extubation? 'Cause a lot of people are uncomfortable with that and they don't do it right away. So short intubation just for maybe hypotension or an airway, when is it safe to take that tube out? - I think these patients can generally be excavated pretty expeditiously because the nice thing about like allergic anaphylaxis is that it comes quickly and then you treat it and oftentimes it seems like it gets better quickly. So I think you can typically excavate these patients the next day once the dust is kind of settled. You wanna wait to see if they have lip swelling or any observer-bull swelling, that can be rough gauge of what's going on. So like when their lips and their tongue look better, you know, their epiglottis is probably a bit better. One maneuver that I like to do if there's any doubt is to deeply sedate the patient and just just really gently put a glidescope or hyper-angulated videolovergar scope in and just kind of take a look at the epiglottis and just get a sense of is it like sharp and nice looking or is it still really bloated? And usually kind of based on the way the lips and the tongue and the epiglottis potentially are looking, you can typically excavate these people within 24 hours. And you might wanna look for a cuff leak or not. And then the other thing I think when it's out, you can excavate them over an airway exchange catheter. So stick an airway exchange catheter and excavate them, make sure that they can breathe and they're not like super striculous and then after five minutes pull out the exchange catheter. - I totally agree. Sometimes I don't even for five minutes use average but I think for sure it's a get out of trouble card easy if the tube comes out and you gotta get one back in right away. - There was one paper done in Hartford where they left these things in for like hours. - Well, I guess the whole point is you've changed one big tube for a little one, but. - Yeah, no, I think it just seems harsh for me. - No, yeah, you're right, realistically, it's probably more like one or two minutes, I don't have that much patience. (upbeat music) (upbeat music) Okay, disposition. So how long do I have to observe them for and let's talk about discharge instructions? Because from my mymerge lens, this bifasic reaction that we're so terrified of, BC in itself, from our Poison Control Center, published an awesome cohort. Retrospective analysis that bifasic reactions are very, very, very rare. Yeah, bifasic reactions are basically recurrent anaphylaxis. They can occur up to somewhere around 72 hours. So all these patients need to be admitted to an ICU and kept in the hospital for 72 hours, preferably with an epinephrine ready to go. Because otherwise they may just explode. True, no one goes home without one or two epipans. Well, I guess in the states, expensive as hell, but one or two epipans at their prescription for their steroids, then of course, really good follow-up and very good reliable friends around them to help them out. Yeah, I'm just messing with you and I, you know, swam in cases listening to, you know, I don't think, at least to my knowledge, and honestly, you know, this better than I do. I don't think there's any good evidence that any specific duration of observation in the hospital is necessary. So I think that's kind of just a clinical decision. I hundred percent agree. Don't tweet us, swam. Don't hate us. All right, Josh, we're the endpoint of the podcast pitfalls. What should I remember at the end of this podcast? So honestly, I think one major pitfall is failing to consider anaphylaxis. Just writing this chapter is terrifying because it can, it can present in all sorts of different ways, like intraoperative anaphylaxis, like you intubate someone in their blood pressure tanks, like probably be like one of the last things I think about usually. So just cap this on your mind, especially when patients are coming in with multiple different organ systems that are acting up or some sort of exposure. And I think, you know, the next major pitfall is fear of using epinephrine or delaying epinephrine. So whether you're more comfortable with IM or IV epinephrine, whatever makes you happier or as faster to get, I think that is a really important therapy, even if the patient's blood pressure is okay, they may potentially beat disease modifying and kind of get you out of trouble. I totally agree. Don't forget to think about this. Rockuronium and deustanaphylaxis is this unicorn and now that I've seen it, I'm freaking terrified, Josh, so planning for it is important. Yeah, and apparently there's also a core hexadeen and deustanaphylaxis. I've never seen that, but that would be so difficult to find. Apparently it's one of the most common antigens causing anaphylaxis in healthcare. Crazy. Terrifying. Yep. All right, Josh. As always, thanks for an awesome post. We're ready for anaphylaxis. Don't forget about it. Throw the kitchens and get them. Don't be afraid of IV epinephrine. All right. Thank you. Thanks.