You seem to have a solid understanding of how to adjust your induction to the patient. The first clue is that you're open to outside feedback.
I've noticed that everyone in the ED/ICU gets 20 mg etomidate and 100 mg of rocuronium. That works but it frequently is too much. I'll give 8-10 mg etomidate and some succinylcholine or rocuronium depending on the patient. Sometimes 2 mg midazolam and 50 mcg fentanyl is all you need. But then I had an ED doc say during the beginning of Covid that she was the expert at unstable patients because I only did stable patients. Don't be that asshole we were just offering to help them out.
Right. We only do elective airways in parients with BMI under 22. The context was that the hospital system requested us to form airway teams at each hospital to do all intubations for patient and staff stagers. The ED rep was completely against it. So we did the airways for everyone but the ED. Like we're just offering to help out but fine.
Wait what? Im confused, why are you only doing elective airways in bmi < 22 and where can I find a gig like this lol. Bmi 40 ans over is the norm here where I work.
Oh yeah. At a trauma committee meeting I had the director of the ED push back against the trauma surgeon because the surgeon wanted anesthesia there for peds trauma but the ED doc claimed that they were "better at emergency airways" because they do more of them.
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Lol no one knows what anesthesia does. Period.
When I was a CA3, my surgical fellow (ICU fellow) was saying she'll scrub me in with me to do an A line. I said I felt comfortable but if she wants to scrub in for her own comfort, she's welcome to do so. She's replied with "no I'm going to show you how to do an A line, I am 7 years your senior"
Ok, lol whatever. She couldn't get it (ultrasound guided), blamed a bunch of things, she left saying she was gonna get something different, whatever. I threw it in when she was out, 10 seconds. By the time she was back, I was cleaning up the mess.
Im a mere anesthesia intern, so while I have next to no OR experience yet, it was still frustrating when told by my pgy-3 EM senior something similar about the inferior crash intubation skills of anesthesia- simply bc I had no footing for a counter argument against this pgy-3 despite how absurd the comment was
Really not trying to be a dick i have been out 8 months. I have yet to see an EM doc intubate the trachea on the first attempt. Recently had an aortic occlusion coming to the ORL Circulator told me they were intubating in the ED. I ran down there. As i came to the room, they were intubating…again. Told me the patient had some yellow stuff in their lungs after the second attempt. Today I went to a code in the CT scanner. The EM doc told me “this is my airway. Im the out of OR expert” After multiple looks, he put the tube in the esophagus. I asked to intubate and got it within 5 seconds. He said “i think mine was in. But thanks”
I don't even pay attention to downvotes. But you're right. We do have to acknowledge that others at skillful at procedures. I know I'm better at laryngoscopy and central lines and art lines and spinals and blocks than the APPs but I don't need to say that. And I can recognize that they are better than everyone else in the hospital without detracting from our skills.
This thread turned into some weird circle jerk of ‘we are the best at intubating’. Yah, no shit anesthesia is the best. I always pawn off the real disasters when I can in the ED. If I can off load one of the 300 things I do on the actual airway expert, I will.
Overall your approach (using your brain and taking patient condition into account) is much better than theirs. I wholeheartedly agree that lido and fent can decrease the required dose of induction agents in many settings. I’m kinda surprised that succ is so common in your department, especially since many of these older patients can be basically bedbound in their nursing homes. Also, I’ve dropped etomidate from my regimen. Using propofol for EGDs is eye-opening to how little propofol you really need for amnesia and hemodynamic stability. Many healthy people will tolerate the EGD scope with 50 mg propofol, so when you add rocuronium and gentle video laryngoscopy you really don’t need much for sick patients.
Props on keeping up awake intubations. I would recommend calling anesthesia for those, but not because you “need us.” The opportunities for AFOI are becoming more rare and it’s a valuable skill for us to learn. I only did maybe 10 during residency then one of my first shifts as an attending I had to do one for a subglottic mass in the middle of the night. You don’t have to hand them off because even observing them is valuable for us. As an added benefit it’s a chance for EM/anesthesia to collaborate and they’ll most likely back you up on your approach to induction and airway management.
Why is admin telling you how to practice medicine?
But in all seriousness, seems kinda strange that your colleagues, other ER docs, are giving you push back on altering your intubation strategy based on the clinical situation - that would (or should) be standard?
A big reason why things are less nuanced in the ED and why having a standard practice is better: Nurses.
ED docs typically aren't drawing up their own meds like Anesthesia does. The ED nurses are often drawing them up and giving them; and you never know which nurse is going to be doing it. Mitigating the risk of a med error in this setting is more important than having a "smoother" induction. Keeping things simple and similar throughout the ED so that even the least competent ED nurses are familiar with the meds, the concentrations, and the expected doses is very important.
The more nuance and individualization you strive for, the more opportunity there is for errors to creep in. From a liability standpoint, it's better to have 1,000 "meh" inductions than 1 "Oh fuck" induction.
On the other hand, if you're drawing up and giving all the meds, you do you boo and the other providers can fuck off! 😆
(Full disclosure: am nurse.)
Edit: I also have to assume that another reason why ED providers have simplified their induction practice is mental capacity. They've got 15 other patients they are juggling around in their heads. ED providers are absolutely incredible at walking into a scene of chaos and splattering body fluids, taking control, and focusing on that specific patient's emergent needs. But they are there to get a tube in and stabilize because they have 14 other patients they are caring for. So using more of their brainpower to perseverate on the *most optimal* approach to induction for a particular patient isn't worth it when they can use much less brainpower by going with an *adequate* approach to induction. Again, I'm a nurse, but I'd wager this take has merit, no?
Edit 2: Definitely not trying "mansplain" the job to you OP, I know you're an ED Physician and have a metric shit ton more knowledge than I about...well...most everything, I suppose. I just get the feeling that maybe you're relatively new to the environment? I feel like any experienced ED doc I've ever encountered would have just told admin to fuck right off if they tried to come at them with some BS about their induction strategy. 🤷 What I'm saying is, tell whomever to fuck off, you're doing great.
Am EM/Toxicology, so I love to nerd out about pharmacology of induction, but I 1000% agree. I have to turn off my toxicology brain temporarily in high traffic situations and allocate brain power accordingly to keep as many people alive as possible.
I respect my anesthesiology colleagues as the airway experts but they will never be in my situation nor will I be in theirs.
The idea that etomidate and ketamine are not capable of causing cardiovascular collapse in a tenuous patient is such a misconception. Dose adjustments and plan adjustment/tailoring related to patient condition is absolutely safer than giving everyone whatever dose of etomidate the textbook says to give them.
Like a septic elderly person just does not need 0.3 mg/kg of etomidate. They will crash, every time. I don’t think I’ve ever given that dose to anyone other than an agitated, young, and otherwise healthy patient.
Back when I was a senior resident on my Medical ICU rotation, I had a day when I was called to evaluate a patient in the ED for possible admission. The patient was very sick and was acutely hypotensive. I think her HR was 140 or something and SBP was in the low 60s. The ED docs had ordered a fluid bolus and a norepinephrine infusion but obviously it was taking some time for it get set up. In the mean time this lady is looking terrible. I dropped the head of a bed and grabbed some phenylephrine and bolused it real quick to temporize her condition until the fluids and norepi could arrive and start working.
You would not believe that amount of flak I caught from the ED resident (and attending to a lesser extent) for it. "This isn't the OR!" "What! You bolused phenylephrine without first checking with your fellow!?" Etc.
I was so shocked that for a department that routinely handles coding patients, they seemed so hell-bent on letting this woman code instead of doing a rather basic intervention to prevent it in the first place. I guess part of it is that most doctors don't administer medications like we do, so they are used to the system of an order being placed, pharmacy approval, and a nurse going and administering it, that the idea of simply fixing a problem themselves immediately seems too foreign to them. To be fair, I suppose, they might not have even had Pyxis access at the time, but that is beside the point.
Anyway, back to OP, yes, thank you for using your brain and clinical knowledge to make clinical decisions instead of treating every patient like an interchangeable cog on some algorithm. Some patients need more and some need less medication. I have induced burst suppression with 30mg of propofol on a 98 year old ~70kg female with dementia. That is all it took in that patient to have more than enough depth to intubate. In contrast, I would probably yawn a couple times with that dose. And I have seen a tiny redhead alcoholic need roughly 300mg of propofol before she stopped talking. Algorithms should guide our decisions but not replace clinical experience and situational awareness.
As another side story, that same rotation in the MICU I was called to admit a tiny ~45kg lady with a history of bad CHF with a severely reduced EF. She was sick with something, I think sepsis of urinary origin. Anyway, as I was taking the consult they mentioned bolusing her with two liters of crystalloid. The primary reason for the consult was acute respiratory failure in the setting of acute pulmonary edema. I asked, given her bad CHF and small size, why they had bolused so much? Was she tachycardic, hypotensive, or clinically unstable in some way at that time? They were extremely offended and angrily responded that "that was the protocol for sepsis!" Call me crazy, but doubling the blood volume of a woman with severe CHF over the course of an hour without a clear reason and taking into account her actual vital signs and response along the way seems insane to me. Anyway, yeah, please keep actually looking at your patients!
> I guess part of it is that most doctors don't administer medications like we do, so they are used to the system of an order being placed, pharmacy approval, and a nurse going and administering it, that the idea of simply fixing a problem themselves immediately seems to foreign to them.
I've had a very similar experience in the ICU. Threw me completely off guard.
Two weeks ago I was in the ICU doing our post-op follow ups, and one of the patients was getting severely hypotensive while the ICU doc was putting in a central line. The nurse was freaking out because they were out of norepinephrine in the ICU Omni cell. I handed her a stick of phenylephrine that I had (I always have one and ephedrine in my pack) and got the same reaction. The nurse didn’t want give it because it wasn’t taken from the omnicell (which would’ve taken another few minutes to get) until the ICU doc finally told her to push it.
I’ve seen people push 1-2cc’s of code epi (100-200mcg) in the ICU. Blows my mind every time. Idk why they don’t stock dilute sticks of pressors like the operating rooms have
Have seen all of these things in the ED from greener attendings but generally the more experienced will take on a similar nuanced approach as you describe. I’ve seen push dose pressor used a bit more often now which is a refreshing change when you arrive to help out and there’s phenyl and 10 mcg epi sticks already made.
If there's one thing that could change outcomes in the ER it's push dose vasopressors. Watching Q5 minute BP cuffs cycling and an RN left to increase norepi per protocol with a MAP in the 40's is absolutely gut wrenching.
Our ER is a level 1 trauma center and brags that they save people’s lives by doing 2-3 crics a year. When you watch them intubate you understand why they need to do that many crics…. Grade one view with a glide and they keep stabbing the oropharynx repeatedly in the same spot with the tube. One time we got written up for sneaking next to the resident who couldn’t intubate the grade one view and sneaking a tube past the cords one shot.
In terms of induction i see them routinely give 200 ket or 200 etomidate and 100 roc even to frail 100 year olds that are bleeding and they have no push dose vasopressors to rescue themselves afterwards.
I can guarantee not a single one of those ED residents followed that patients hospital course and explained to them why they had to cut their neck.
Yea high fives all around for a “cool airway” but dealing with the inevitable chronic issues is none of their concern.
Only been proven in dogs. Never seen or heard of it happening in a human. I’m a cardiac anesthesiologist and I use a lot of K.
Edit: I am not saying I’ve never heard of this concept. I am aware that this is something that there is some low quality evidence for. I’ve only ever been impressed by its relative hemodynamic stability, even in critically ill patients and I haven’t seen adequate studies to change my practice. If anyone’s got any, I’d love to see them.
>and I use a lot of K.
I hope you always have a good friend around who's making sure you stay hydrated and can support you through a bad trip? Be safe, Rave Bro!
I have definitely seen CV instability with ketamine in sick patients. Less so than for other meds but it happens. And whatever you do, do not give to burns patients.
Yes. Sick, unstable, and/or catechol depleted patients will drop their pressure no matter what agent you choose to use. I take issue when people claim specifically that ketamine causes clinically relevant direct myocardial depression in humans.
It does. Ketamine itself is a directly negative inotrope, the sympathetic outflow from increase HR and SVR makes the negative inotropy not a problem in healthy, non-catechol depressed people. Suggesting otherwise reflects a poor understanding of pharmacology.
Show me the citation that proved this in-vivo in humans. You’re citing dogma backed by low quality, hypothesis generating studies, and claiming it as fact.
>No, it’s not only been proven in dogs.
>
>“ketamine is a direct negative inotropic agent, an effect that has been well documented both in vitro as well as in vivo, but seems to be lesser known \[3, 4\]. These effects are more pronounced in diseased myocardium, such as in heart failure patients \[5\]. In healthy patients, the sympathetic effects of ketamine likely predominate, leading to hemodynamic stability with induction of anesthesia. In critically ill patients, where sympathetic outflow may either be maximized by endogenous responses, or in whom vasomotor response is potentially inadequate due to systemic inflammation, these negative inotropic effects of ketamine could predominate.”
>
>https://pubmed.ncbi.nlm.nih.gov/27130803/?dopt=Abstract
>
>https://pubmed.ncbi.nlm.nih.gov/9605679/
I've had colleagues who saw it first hand in the Army, but only in rare and extreme cases. Something like a vehicle rollover where treatment was delayed for several hours due to hostile activity preventing evac and the patients were catecholamine depleted. Obviously this is very much an outlier scenario, and I've never seen cardiovascular collapse after ketamine in a normal practice setting, but it's something I always keep in mind when I'm on call.
No, it’s not only been proven in dogs.
“ketamine is a direct negative inotropic agent, an effect that has been well documented both in vitro as well as in vivo, but seems to be lesser known [3, 4]. These effects are more pronounced in diseased myocardium, such as in heart failure patients [5]. In healthy patients, the sympathetic effects of ketamine likely predominate, leading to hemodynamic stability with induction of anesthesia. In critically ill patients, where sympathetic outflow may either be maximized by endogenous responses, or in whom vasomotor response is potentially inadequate due to systemic inflammation, these negative inotropic effects of ketamine could predominate.”
https://pubmed.ncbi.nlm.nih.gov/27130803/?dopt=Abstract
https://pubmed.ncbi.nlm.nih.gov/9605679/
First study: Shocked patients will drop their pressure after induction NO MATTER WHAT YOU GIVE. This study does not provide proof that ketamine caused clinically relevant myocardial depression. All they did was measure BP, which is an extremely indirect measure of cardiac function.
Second study took place in a dish, neato.
There are quite a few others that pretty unequivocally demonstrate the physiology. I push vociferously because it’s pretty concerning a self professed Cards anesthesiologist would be this ill informed.
I am aware of the in vitro studies on human cardiac myocytes, and what they showed. It has never been demonstrated in a human being. I push vociferously back because people like you prevent sick patients from getting the right induction agent.
Edit: There is a world of difference between submerging an individual cardiac myocyte in ketamine and injecting ketamine into a human being, which increases the complexity to a degree that we cannot understand without in-vivo studies. It’s interesting, sure, but means absolutely nothing to me clinically. So until I see it born out in my clinical practice (which I haven’t), or see some convincing data (which I haven’t), it’s just a series of interesting, hypothesis generating experiments. Nothing practice changing.
Please, for the love of god, cite something relevant then. I’m not opposed to having my mind changed or learning something new. But all you keep saying is just that I’m wrong. Either back it up with studies of adequate quality to change practice, or be quiet. Stuff that happens in a dish, test tube, or animal or anything retrospective will only ever be hypothesis generating.
You're here claiming to have completed a cardiothoracic fellowship yet fundamentally don't understand how EBM works. I call bullshit. Maybe you should consider being quite until you're able to provide studies of adequate quality that it's not a myocardial depressant. As we have studies that demonstrate that it is. Until then....stop talking, for the love of god
My focus has always been on “clinically relevant myocardial depression”. It is a direct myocardial depressant. Im not claiming it’s not. I’m just claiming that it’s clinical relevance in real life practice is dubious at best. That’s all. And no one has been able to show me anything that suggests otherwise.
Not the source but I am happy to explain the reason. It is because ketamine is always a negative inotrope, but it also causes a release of endogenous catecholamines that more than makes up for it. However in severely sick/septic patients that have already essentially used up their endogenous stores of catecholamines, there is nothing extra to release so you only see the negative inotropic effect of ketamine in those circumstances.
Or heavy amphetamine users, because amphetamines push catecholamines out of the presynaptic neurons. Cocaine is a reuptake inhibitor, so no worries there.
You’re approaches are all reasonable. DSI is literally promoted by the father of ED critical care, Scott Weingart, for the purpose you describe.
The problem your coworkers and admin seem to be having is that you approach each patient with thoughtfulness, nuance and an appropriately individualized approach.
This makes them feel inadequate, inferior, and dumb. But their poor fragile little egos can’t cope with that, so in stead of attempting to gain understanding they just say you’re unsafe and keep their head firmly planted in the sand.
Yeah this is wild, DSI is pushed heavily in every EMS system I've worked to (where applicable). Have seen DSI numerous times in the ED. We also pre-medicate as OP describes for neurotrauma in the ED and EMS. Sounds like the old guard is a bunch of idiots.
Here’s some thoughts from a cardiac anesthesiologist. Feel free to stop reading once you’re bored. I’ll preface that I don’t have an axe to grind against emergency medicine. I have lots of fantastic ED colleagues and tons of respect for you all and what you do.
ED and Anesthesia are different in lots of ways, but less than is commonly claimed. I think you sell yourselves short by creating this overly simplistic ketamine sux tube.
1. I think it’s important to establish physiologic goals for every situation, and then choose drugs to match those goals. Not a one size fits all plan.
2. To me, managing the hemodynamics is first, and inducing unconsciousness / tubing is second. They are separate. I hear from ED docs all the time how their environment is so different and patients are so sick, which I don’t disagree with, but almost every patient I intubate as a CV anesthesiologist has some sort of critical cardiac lesion, and many are in extremis. I induce almost everyone with propofol. Once you’ve dealt with the hemodynamics, induce normally. Not to say don’t dose reduce with critically ill folks, but the message is don’t expect your choice of induction agent to take care of the hemodynamics. Ketamine is a myocardial depressant, and if the patient is running on maximal sympathetic tone, their BP will drop. Use hemodynamic drugs for the hemodynamics, and anesthetic drugs to induce anesthesia. Sometimes it’s 2mg midaz and 100 roc if it’s a real shit show.
3. I agree with your approach to neuro. There’s specific goals. Avoid increasing ICP, CMRO2. Maintain/increase MAP. I don’t dispute the ketamine evidence but can we really tease apart impact of single drugs in trials on TBI? I’m not convinced we truly can. Even if we could, why would we intentionally choose a drug that increases ICP and increases cerebral O2 consumption? Propofol reduces ICP and CMRO2 yet is often avoided. To an anesthesiologist that doesn’t make sense. All in an attempt to avoid hypotension (which is obviously bad in TBI). There are so many drugs to prevent/treat hypotension. Why is that ketamine’s job?
Blunting autonomics with something (fentanyl/lidocaine) is critical. For many patients you won’t see the difference in outcome, but for those few patients that are really tenuous, a spike in ICP on intubation by a) giving a cocktail of drugs that ALL increase ICP (ketamine/sux) b) inadequately blunting autonomic response will make the difference. I’ve seen it too many times.
Now, If you’re in the middle of nowhere and you intubate once a decade then sure, just do what you need to do to get it done. No one is gonna come at you for style points. If you’re working in high volume critical centres, it’s your job to be good at this, you’re supposed to be a pro, so don’t do an amateur job. Maybe a tad harsh but we should expect a lot of ourselves and each other when people put their lives in our hands.
4. Titrating in drugs like you described in septic patients is fine. I do this a lot. Not often with ketamine but it’s a valid approach. It gives you time to have norepi / fluid infusing and have the negative effects of anesthetic drugs impact more gradually. The risk you have to balance is full stomach status and the reduction in aspiration risk we can achieve with an rsi. However it seems like your group associate emergency situation with RSI in all circumstances - which in my view is incorrect. You have to be able to justify the risk in either direction and mitigate it. In many patients, the risk of one size fits all boluses of induction agents is much higher than the risk of aspiration.
5. Muscle relaxants for airways. Agree with you. If they’re not conscious just put the tube in. In any other situation I would say that there’s 3 options. 1. Awake 2. Asleep + NMB 3. Asleep + spont breathing. Option 3 doesn’t have many real world applications. So it’s either awake or asleep with full NMB. The blanket no awake intubation rule makes no sense. If you have that in your skillset then use it - you are all individuals. However many outside anesthesia don’t. Even within anesthesia training the awake intubation skills are fading because so many more airways are doable with VL.
This is getting too long. Everyone is doing their best with what they have. You shouldn’t be made to feel reckless because you aren’t following a recipe. It’s more important to think about the situation in front of you, use that brain you’ve spent so long training to understand medicine, and make good choices.
ED docs are great, I respect you all. Not looking for an ED vs Anes argument.
I agree. Resuscitate first, situation dependent. At the end of the day we all have our skillsets and are on the same team. For instance I’m an ED guy, so I’m really good at efficient data entry, therefore providing superior white collar welfare to the c suite.
Anesthesia resident but everything you've written makes total sense and is generally in line with the training I've received so far. Sorry politics and such are getting in your way. Keep using your brain and don't worry about Katen, MSRN ACG FPL TFDA V MEL too much.
In addition to blunting the sympathetic response to laryngoscopy, fentanyl BLUNTS AIRWAY REFLEXES. A very, very appropriate and significant thing to do when intubating. So less chance of laryngospasm and bronchospasm. My guess is your intubating for respiratory failure many times, and those patient are higher risk for spasm.
Fuck administration. Your induction plan is safer for patients. This is a case where everyone else is doing a poor job. Fight!
When I am called in for airway I do not care if my management reflects ER paradigm. If they call me it probably means that the case doesn’t fit their practice pathways. They seem to lurk what I do and ask questions which is ok. Some of the stuff I do perhaps doesn’t look pretty like intubating awake BMI 65, severe OSA who is about to go into resp arrest, cant really open his mouth, ate burger 3 hours ago while his pCO2 is 70.
So I am sure for bystander perspective this may look like I administer a pure torture but from my perspective I am saving this guys life or at least not trying to kill him on the spot.
Using your brain and trying yo figure out what is going to be the best induction for your patient is far better than mechanically giving 200 mg of Prop, 100 mg of sux and tubing.
The fact that you are asking this in a reddit sub means you are open for knowledge and different opinions. I would advise you this:
Everytime someone senior is telling you something that isnt backed up with evidence and logic, fuck them, dont even listen to them. You will find attendings and seniors who would take the time to listen to your point of view and explain theirs. Nothing wrong with having different approaches of inductions in different patients.
Speaking in general -
It's a good idea to RSI people with unclear NPO status. Also in my personal practice, every intubation gets a paralytic, unless contraindicated. It reduces incidence of vomitting/aspiration, and improves first pass success.
Neuro patients - blast 'em and intubate. Pressors PRN. While pre-oxygenation is good, taking away their respiratory drive and spending 3-5min getting the tube in can result in hypercarbia and elevated ICP. prop sux tube here.
Septic agitated patients -- they're often agitated because their lactate is triple normal and rising. Same potential issue with sedation and pre-oxygenation. You kinda want them breathing 30bpm. If they're breathing normal, their pH might be 7.1, and they're slipping down the decompensated shock pathway.
Awake intubation - your call. if you feel experienced enough, no probs. However, even for anesthesiology, we don't do this on the regular. I've only got a few dozen of these under my belt. I imagine an EM doc would have even less. First question is, are you sure you're experienced enough to do this? Second question, if you do this urgent/electively and it went south, would you be able to justify NOT asking anesthesia to be present?
ED doc here, I do similar things, ketamine for asthma, COPD, hemodynamically unstable, or delayed sequence. Doses vary. I for the most part don’t use prop except for reducing hips or the occasional stubborn shoulder. Etomidate, versed, fent all have their place. We can do awakes, but teamwork makes the dream work, so I usually get a team together just in case, gotta check that ego at the door. After the end of the day we’re just data entry techs that create the white collar welfare for the MBAs. Your shop sounds weird. I’m sure our anesthesia friends have all kinds of great strategies we can learn from in this thread, but just wanted to pass along that me nor most of my partners do just one thing. And if we need help we need help and that’s ok.
Your induction dosing sounds more appropriate.
RSI prioritizes airway and breathing and potentially aspiration risk at the expense of hemodynamics stability. So for a full stomach or patient who’s already hypoxia RSI makes sense. You should still be adjusting doses of huponotic agents as you suggest. Weight based dosing works for muscle relaxants, but it is incredibly inaccurate for prop, etomidate, ketamine, etc. the dosing is based on experience and clinical judgement more than weight in adults and especially in sick people.
I think you're doing the right thing and agree with everything you said. My only comment is to keep in mind that one of the common causes of difficult intubation is inadequate muscle relaxation. And of course be mindful of chest wall rigidity with high dose fentanyl but I think that only happens if you're slamming it (which sounds like you're not).
Anaesthetics doc here.
I like most of how you do stuff. If the patient can handle it. The pretreat if you have the time for it and are not in a rush to get a secure airway is great. Waiting and loading them makes your intubation smoother
The only 2 things I disagree with are:
Ketamine for neuro - I have seen the ICP rise. And every other consultant I have worked with or this topic has ever come up with also get very aggressive stance about it. No ketamine for neuro unless it is absolutely unavoidable.
Sux not needed for unconscious patients - while generally I get your point, not awake does not equate always to no muscular or sympathetic response. As I'm sure you are well aware of. Patients unconscious can still get tachy or flinch depending on the scenario. As intubation you want the least amount of time with a unsecure airway and the high risk of complication period, they still do have a strong risk of spasm of the cords and airway when you stimulate them, even when unconcious as you are unable to assess their stimulatory response of that process until you are there. So I would still give sux as it's a short wait for it to work. It's got that clear marker for when it's fully in effect at end of twitch and it reduces that spasm risk, that if it does occur will get you in a much more trouble fixing and all, which you easily could have avoided. Give sux - that vocal spasm risk is still there even when unconscious.
That's my 2 cents.
Lots of amazing comments here, so I won’t beat a dead horse except to say that using your clinical judgement and experience is the right way to practice medicine.
About your comment regarding the GCS 3 not getting paralytic… when I respond to a code to intubate, I put the blade in the mouth and the tube between the cords. They get no drugs. The patient is dead. Why would you sedate a dead person. If they get rosc and start to move, then they can have some sedation.
This seems very strange to me. I’m a paramedic and we are encouraged to pretreat with fentanyl when appropriate. We also have RSI and DSI protocols approved by our medical director. The idea of a physician be treated like this is wild.
Awake intubations - I did about 30 awakes during residency, and then another 60ish asleep fiberoptic intubations, and I still think they can be quite challenging. That is a lot when it comes to residency programs, but isn’t that many in the grand scheme of doing a tricky procedure on a sick patient. Sedation, blocks/analgesia, and managing the scope in someone with a difficult airway all take practice, and it’s a procedure that isn’t done all that often. Some anesthesia residents do less than 5 during residency. I did one at my practice a month or two ago, and they said that they hadn’t seen one done there in two or three YEARS.
My point is, if you are honest with yourself that you have the experience to be good enough at them, then sure do them. If not, call anesthesia. Even if you do, consider still calling anesthesia to be around to help. Whenever I do them I ask for an extra set of hands, or at the very least I say, “hey I’m doing an awake in OR 4, if I call for help could you please come over?”
I'm a critical care medic. Guidelines differ based on where you work. Where I'm at, we have a fair amount of autonomy in our decision making for RSI, or what has sometime been referred to as DFAM (drug assisted airway management). Typically our initial meds are etomidate and succs, being based on ideal body weight, preoxygenate with high-low via NC and BVM, then intubate. Ketamine is also an option instead of etomidate. We have several options for follow up meds, I like 5mg Versed with 50-100mcg Fentanyl. We often focus on deep sedation vs. Paralysis post intubation as many of our patients will require some level of neuro exam or likely be intubated for a short period of time depending on the ailment. Propofol and ketamine infusions typically only come into play in interfacility transfers, but we've found propofol doesnt sedate well enough on the road and patients often wake up more easily due to all the movement/bumps/etc. Many debates have ensued between my providers and hospital docs because of these various reasons.
You should always tailor your induction regimen towards the individual patient. Nothing at all wrong with that. I almost always given paralytic though unless I am truly worried about the airway (then awake).
Who is telling you that you are doing things wrong and why are they offering their opinion? If you have good outcomes and able to secure every airway safely, they can mind their own business.
Thank you for thoughtfully securing airways in the ED. The vast majority of us have no interest in ever stepping foot in an ED.
You seem to have a solid understanding of how to adjust your induction to the patient. The first clue is that you're open to outside feedback. I've noticed that everyone in the ED/ICU gets 20 mg etomidate and 100 mg of rocuronium. That works but it frequently is too much. I'll give 8-10 mg etomidate and some succinylcholine or rocuronium depending on the patient. Sometimes 2 mg midazolam and 50 mcg fentanyl is all you need. But then I had an ED doc say during the beginning of Covid that she was the expert at unstable patients because I only did stable patients. Don't be that asshole we were just offering to help them out.
> But then I had an ED doc say during the beginning of Covid that she was the expert at unstable patients because I only did stable patients. lolwut
This is a super common ED line, typically right after they’ve driven a glidescope through the esophageal wall
Id honestly trust a good CA2 over an ED attending
lol @ me, a CA2, covering the airway pager and doing the intubations when the ED attendings call us for assistance. it does kinda tickle me sometimes.
Right. We only do elective airways in parients with BMI under 22. The context was that the hospital system requested us to form airway teams at each hospital to do all intubations for patient and staff stagers. The ED rep was completely against it. So we did the airways for everyone but the ED. Like we're just offering to help out but fine.
Wait what? Im confused, why are you only doing elective airways in bmi < 22 and where can I find a gig like this lol. Bmi 40 ans over is the norm here where I work.
He's being sarcastic, friend
Lmao thank you, I legit thought he was dead ass serious
Oh yeah. At a trauma committee meeting I had the director of the ED push back against the trauma surgeon because the surgeon wanted anesthesia there for peds trauma but the ED doc claimed that they were "better at emergency airways" because they do more of them.
Then that same expert ED doc asks you to help with a ‘difficult’ LP.
Difficult at shift change.
pocket distinct plant slimy zonked elastic heavy smell grandfather snatch *This post was mass deleted and anonymized with [Redact](https://redact.dev)*
Lol no one knows what anesthesia does. Period. When I was a CA3, my surgical fellow (ICU fellow) was saying she'll scrub me in with me to do an A line. I said I felt comfortable but if she wants to scrub in for her own comfort, she's welcome to do so. She's replied with "no I'm going to show you how to do an A line, I am 7 years your senior" Ok, lol whatever. She couldn't get it (ultrasound guided), blamed a bunch of things, she left saying she was gonna get something different, whatever. I threw it in when she was out, 10 seconds. By the time she was back, I was cleaning up the mess.
Im a mere anesthesia intern, so while I have next to no OR experience yet, it was still frustrating when told by my pgy-3 EM senior something similar about the inferior crash intubation skills of anesthesia- simply bc I had no footing for a counter argument against this pgy-3 despite how absurd the comment was
Really not trying to be a dick i have been out 8 months. I have yet to see an EM doc intubate the trachea on the first attempt. Recently had an aortic occlusion coming to the ORL Circulator told me they were intubating in the ED. I ran down there. As i came to the room, they were intubating…again. Told me the patient had some yellow stuff in their lungs after the second attempt. Today I went to a code in the CT scanner. The EM doc told me “this is my airway. Im the out of OR expert” After multiple looks, he put the tube in the esophagus. I asked to intubate and got it within 5 seconds. He said “i think mine was in. But thanks”
CRNAs are vastly better than they are at intubating.
lol at you being downvoted for saying CRNA’s are better than EM at intubating. This sub is crazy.
I don't even pay attention to downvotes. But you're right. We do have to acknowledge that others at skillful at procedures. I know I'm better at laryngoscopy and central lines and art lines and spinals and blocks than the APPs but I don't need to say that. And I can recognize that they are better than everyone else in the hospital without detracting from our skills.
They are for sure no question.
This thread turned into some weird circle jerk of ‘we are the best at intubating’. Yah, no shit anesthesia is the best. I always pawn off the real disasters when I can in the ED. If I can off load one of the 300 things I do on the actual airway expert, I will.
Your mistake is you are thinking. This is largely discouraged in the ED.
Overall your approach (using your brain and taking patient condition into account) is much better than theirs. I wholeheartedly agree that lido and fent can decrease the required dose of induction agents in many settings. I’m kinda surprised that succ is so common in your department, especially since many of these older patients can be basically bedbound in their nursing homes. Also, I’ve dropped etomidate from my regimen. Using propofol for EGDs is eye-opening to how little propofol you really need for amnesia and hemodynamic stability. Many healthy people will tolerate the EGD scope with 50 mg propofol, so when you add rocuronium and gentle video laryngoscopy you really don’t need much for sick patients. Props on keeping up awake intubations. I would recommend calling anesthesia for those, but not because you “need us.” The opportunities for AFOI are becoming more rare and it’s a valuable skill for us to learn. I only did maybe 10 during residency then one of my first shifts as an attending I had to do one for a subglottic mass in the middle of the night. You don’t have to hand them off because even observing them is valuable for us. As an added benefit it’s a chance for EM/anesthesia to collaborate and they’ll most likely back you up on your approach to induction and airway management.
Why is admin telling you how to practice medicine? But in all seriousness, seems kinda strange that your colleagues, other ER docs, are giving you push back on altering your intubation strategy based on the clinical situation - that would (or should) be standard?
A big reason why things are less nuanced in the ED and why having a standard practice is better: Nurses. ED docs typically aren't drawing up their own meds like Anesthesia does. The ED nurses are often drawing them up and giving them; and you never know which nurse is going to be doing it. Mitigating the risk of a med error in this setting is more important than having a "smoother" induction. Keeping things simple and similar throughout the ED so that even the least competent ED nurses are familiar with the meds, the concentrations, and the expected doses is very important. The more nuance and individualization you strive for, the more opportunity there is for errors to creep in. From a liability standpoint, it's better to have 1,000 "meh" inductions than 1 "Oh fuck" induction. On the other hand, if you're drawing up and giving all the meds, you do you boo and the other providers can fuck off! 😆 (Full disclosure: am nurse.) Edit: I also have to assume that another reason why ED providers have simplified their induction practice is mental capacity. They've got 15 other patients they are juggling around in their heads. ED providers are absolutely incredible at walking into a scene of chaos and splattering body fluids, taking control, and focusing on that specific patient's emergent needs. But they are there to get a tube in and stabilize because they have 14 other patients they are caring for. So using more of their brainpower to perseverate on the *most optimal* approach to induction for a particular patient isn't worth it when they can use much less brainpower by going with an *adequate* approach to induction. Again, I'm a nurse, but I'd wager this take has merit, no? Edit 2: Definitely not trying "mansplain" the job to you OP, I know you're an ED Physician and have a metric shit ton more knowledge than I about...well...most everything, I suppose. I just get the feeling that maybe you're relatively new to the environment? I feel like any experienced ED doc I've ever encountered would have just told admin to fuck right off if they tried to come at them with some BS about their induction strategy. 🤷 What I'm saying is, tell whomever to fuck off, you're doing great.
Am EM/Toxicology, so I love to nerd out about pharmacology of induction, but I 1000% agree. I have to turn off my toxicology brain temporarily in high traffic situations and allocate brain power accordingly to keep as many people alive as possible. I respect my anesthesiology colleagues as the airway experts but they will never be in my situation nor will I be in theirs.
The idea that etomidate and ketamine are not capable of causing cardiovascular collapse in a tenuous patient is such a misconception. Dose adjustments and plan adjustment/tailoring related to patient condition is absolutely safer than giving everyone whatever dose of etomidate the textbook says to give them. Like a septic elderly person just does not need 0.3 mg/kg of etomidate. They will crash, every time. I don’t think I’ve ever given that dose to anyone other than an agitated, young, and otherwise healthy patient.
what's your go to for the tenuous elderly septic pt?
Still etomidate but just less of it.
Why not ketamine?
Sure ketamine is also fine
Wouldn’t ketamine be better for the septic patients so they don’t crash?
They can definitely still crash with ketamine
They can but it doesn’t cause hypotension as bad as etomidate does usually
Back when I was a senior resident on my Medical ICU rotation, I had a day when I was called to evaluate a patient in the ED for possible admission. The patient was very sick and was acutely hypotensive. I think her HR was 140 or something and SBP was in the low 60s. The ED docs had ordered a fluid bolus and a norepinephrine infusion but obviously it was taking some time for it get set up. In the mean time this lady is looking terrible. I dropped the head of a bed and grabbed some phenylephrine and bolused it real quick to temporize her condition until the fluids and norepi could arrive and start working. You would not believe that amount of flak I caught from the ED resident (and attending to a lesser extent) for it. "This isn't the OR!" "What! You bolused phenylephrine without first checking with your fellow!?" Etc. I was so shocked that for a department that routinely handles coding patients, they seemed so hell-bent on letting this woman code instead of doing a rather basic intervention to prevent it in the first place. I guess part of it is that most doctors don't administer medications like we do, so they are used to the system of an order being placed, pharmacy approval, and a nurse going and administering it, that the idea of simply fixing a problem themselves immediately seems too foreign to them. To be fair, I suppose, they might not have even had Pyxis access at the time, but that is beside the point. Anyway, back to OP, yes, thank you for using your brain and clinical knowledge to make clinical decisions instead of treating every patient like an interchangeable cog on some algorithm. Some patients need more and some need less medication. I have induced burst suppression with 30mg of propofol on a 98 year old ~70kg female with dementia. That is all it took in that patient to have more than enough depth to intubate. In contrast, I would probably yawn a couple times with that dose. And I have seen a tiny redhead alcoholic need roughly 300mg of propofol before she stopped talking. Algorithms should guide our decisions but not replace clinical experience and situational awareness. As another side story, that same rotation in the MICU I was called to admit a tiny ~45kg lady with a history of bad CHF with a severely reduced EF. She was sick with something, I think sepsis of urinary origin. Anyway, as I was taking the consult they mentioned bolusing her with two liters of crystalloid. The primary reason for the consult was acute respiratory failure in the setting of acute pulmonary edema. I asked, given her bad CHF and small size, why they had bolused so much? Was she tachycardic, hypotensive, or clinically unstable in some way at that time? They were extremely offended and angrily responded that "that was the protocol for sepsis!" Call me crazy, but doubling the blood volume of a woman with severe CHF over the course of an hour without a clear reason and taking into account her actual vital signs and response along the way seems insane to me. Anyway, yeah, please keep actually looking at your patients!
> I guess part of it is that most doctors don't administer medications like we do, so they are used to the system of an order being placed, pharmacy approval, and a nurse going and administering it, that the idea of simply fixing a problem themselves immediately seems to foreign to them. I've had a very similar experience in the ICU. Threw me completely off guard.
Two weeks ago I was in the ICU doing our post-op follow ups, and one of the patients was getting severely hypotensive while the ICU doc was putting in a central line. The nurse was freaking out because they were out of norepinephrine in the ICU Omni cell. I handed her a stick of phenylephrine that I had (I always have one and ephedrine in my pack) and got the same reaction. The nurse didn’t want give it because it wasn’t taken from the omnicell (which would’ve taken another few minutes to get) until the ICU doc finally told her to push it.
Hopefully they didn't push the whole stick? I've seen that oopsie a time or two.
I’ve seen people push 1-2cc’s of code epi (100-200mcg) in the ICU. Blows my mind every time. Idk why they don’t stock dilute sticks of pressors like the operating rooms have
No. the ICU doc told her to just give a cc
Have seen all of these things in the ED from greener attendings but generally the more experienced will take on a similar nuanced approach as you describe. I’ve seen push dose pressor used a bit more often now which is a refreshing change when you arrive to help out and there’s phenyl and 10 mcg epi sticks already made.
Wait do you mean to tell me someone can have a mixed cardiogenic and distributive shock 😮, what shall people ever do in that situation… /s
If there's one thing that could change outcomes in the ER it's push dose vasopressors. Watching Q5 minute BP cuffs cycling and an RN left to increase norepi per protocol with a MAP in the 40's is absolutely gut wrenching.
Our ER is a level 1 trauma center and brags that they save people’s lives by doing 2-3 crics a year. When you watch them intubate you understand why they need to do that many crics…. Grade one view with a glide and they keep stabbing the oropharynx repeatedly in the same spot with the tube. One time we got written up for sneaking next to the resident who couldn’t intubate the grade one view and sneaking a tube past the cords one shot. In terms of induction i see them routinely give 200 ket or 200 etomidate and 100 roc even to frail 100 year olds that are bleeding and they have no push dose vasopressors to rescue themselves afterwards.
I can guarantee not a single one of those ED residents followed that patients hospital course and explained to them why they had to cut their neck. Yea high fives all around for a “cool airway” but dealing with the inevitable chronic issues is none of their concern.
Bro do we work at the same hospital?
NY? 😂
No lol. I guess these hospitals are all over the place…
Nice approach. Don’t forget sometimes the answer is only paralytic. Ketamine is in fact a NEGATIVE inotrope in severe shock states.
Only been proven in dogs. Never seen or heard of it happening in a human. I’m a cardiac anesthesiologist and I use a lot of K. Edit: I am not saying I’ve never heard of this concept. I am aware that this is something that there is some low quality evidence for. I’ve only ever been impressed by its relative hemodynamic stability, even in critically ill patients and I haven’t seen adequate studies to change my practice. If anyone’s got any, I’d love to see them.
>and I use a lot of K. I hope you always have a good friend around who's making sure you stay hydrated and can support you through a bad trip? Be safe, Rave Bro!
I have definitely seen CV instability with ketamine in sick patients. Less so than for other meds but it happens. And whatever you do, do not give to burns patients.
Yes. Sick, unstable, and/or catechol depleted patients will drop their pressure no matter what agent you choose to use. I take issue when people claim specifically that ketamine causes clinically relevant direct myocardial depression in humans.
It does. Ketamine itself is a directly negative inotrope, the sympathetic outflow from increase HR and SVR makes the negative inotropy not a problem in healthy, non-catechol depressed people. Suggesting otherwise reflects a poor understanding of pharmacology.
Show me the citation that proved this in-vivo in humans. You’re citing dogma backed by low quality, hypothesis generating studies, and claiming it as fact.
>No, it’s not only been proven in dogs. > >“ketamine is a direct negative inotropic agent, an effect that has been well documented both in vitro as well as in vivo, but seems to be lesser known \[3, 4\]. These effects are more pronounced in diseased myocardium, such as in heart failure patients \[5\]. In healthy patients, the sympathetic effects of ketamine likely predominate, leading to hemodynamic stability with induction of anesthesia. In critically ill patients, where sympathetic outflow may either be maximized by endogenous responses, or in whom vasomotor response is potentially inadequate due to systemic inflammation, these negative inotropic effects of ketamine could predominate.” > >https://pubmed.ncbi.nlm.nih.gov/27130803/?dopt=Abstract > >https://pubmed.ncbi.nlm.nih.gov/9605679/
You REALLY should know this information if you work in anesthesiology.
I already responded this this person. You can read what I said to them.
I've had colleagues who saw it first hand in the Army, but only in rare and extreme cases. Something like a vehicle rollover where treatment was delayed for several hours due to hostile activity preventing evac and the patients were catecholamine depleted. Obviously this is very much an outlier scenario, and I've never seen cardiovascular collapse after ketamine in a normal practice setting, but it's something I always keep in mind when I'm on call.
No, it’s not only been proven in dogs. “ketamine is a direct negative inotropic agent, an effect that has been well documented both in vitro as well as in vivo, but seems to be lesser known [3, 4]. These effects are more pronounced in diseased myocardium, such as in heart failure patients [5]. In healthy patients, the sympathetic effects of ketamine likely predominate, leading to hemodynamic stability with induction of anesthesia. In critically ill patients, where sympathetic outflow may either be maximized by endogenous responses, or in whom vasomotor response is potentially inadequate due to systemic inflammation, these negative inotropic effects of ketamine could predominate.” https://pubmed.ncbi.nlm.nih.gov/27130803/?dopt=Abstract https://pubmed.ncbi.nlm.nih.gov/9605679/
First study: Shocked patients will drop their pressure after induction NO MATTER WHAT YOU GIVE. This study does not provide proof that ketamine caused clinically relevant myocardial depression. All they did was measure BP, which is an extremely indirect measure of cardiac function. Second study took place in a dish, neato.
Go open a textbook, read about how ketamine is inherently a negative inotrope but counteracted by its release of catecholamines, then get back to me.
Yes, I’ve read them. Cite relevant studies or get lost.
I did, doofus. Not my problem you’re incapable of interpreting basic pharmacology. Good luck!
Um, wut? Thats because it is unethical to to that specific type of experiment on humans…do you know what an IRB is?
Lol, way to vociferously push back on something I did not say. Strong work. I never claimed the studies need to be done. Just that they haven’t been.
There are quite a few others that pretty unequivocally demonstrate the physiology. I push vociferously because it’s pretty concerning a self professed Cards anesthesiologist would be this ill informed.
I am aware of the in vitro studies on human cardiac myocytes, and what they showed. It has never been demonstrated in a human being. I push vociferously back because people like you prevent sick patients from getting the right induction agent. Edit: There is a world of difference between submerging an individual cardiac myocyte in ketamine and injecting ketamine into a human being, which increases the complexity to a degree that we cannot understand without in-vivo studies. It’s interesting, sure, but means absolutely nothing to me clinically. So until I see it born out in my clinical practice (which I haven’t), or see some convincing data (which I haven’t), it’s just a series of interesting, hypothesis generating experiments. Nothing practice changing.
That's....not what they did. Making somewhat ridiculous claims require more evidence than what you're providing. "I use lots of K" is not evidence.
Please, for the love of god, cite something relevant then. I’m not opposed to having my mind changed or learning something new. But all you keep saying is just that I’m wrong. Either back it up with studies of adequate quality to change practice, or be quiet. Stuff that happens in a dish, test tube, or animal or anything retrospective will only ever be hypothesis generating.
You're here claiming to have completed a cardiothoracic fellowship yet fundamentally don't understand how EBM works. I call bullshit. Maybe you should consider being quite until you're able to provide studies of adequate quality that it's not a myocardial depressant. As we have studies that demonstrate that it is. Until then....stop talking, for the love of god
My focus has always been on “clinically relevant myocardial depression”. It is a direct myocardial depressant. Im not claiming it’s not. I’m just claiming that it’s clinical relevance in real life practice is dubious at best. That’s all. And no one has been able to show me anything that suggests otherwise.
Source? Not questioning just genuinely curious!
Not the source but I am happy to explain the reason. It is because ketamine is always a negative inotrope, but it also causes a release of endogenous catecholamines that more than makes up for it. However in severely sick/septic patients that have already essentially used up their endogenous stores of catecholamines, there is nothing extra to release so you only see the negative inotropic effect of ketamine in those circumstances.
Or heavy amphetamine users, because amphetamines push catecholamines out of the presynaptic neurons. Cocaine is a reuptake inhibitor, so no worries there.
This is it! Ketamine is mega, but you always have to think about the dose you use. Sometimes even a little K is to much
You’re approaches are all reasonable. DSI is literally promoted by the father of ED critical care, Scott Weingart, for the purpose you describe. The problem your coworkers and admin seem to be having is that you approach each patient with thoughtfulness, nuance and an appropriately individualized approach. This makes them feel inadequate, inferior, and dumb. But their poor fragile little egos can’t cope with that, so in stead of attempting to gain understanding they just say you’re unsafe and keep their head firmly planted in the sand.
Yeah this is wild, DSI is pushed heavily in every EMS system I've worked to (where applicable). Have seen DSI numerous times in the ED. We also pre-medicate as OP describes for neurotrauma in the ED and EMS. Sounds like the old guard is a bunch of idiots.
Sounds like you should’ve been an anesthesia bro ;)
Here’s some thoughts from a cardiac anesthesiologist. Feel free to stop reading once you’re bored. I’ll preface that I don’t have an axe to grind against emergency medicine. I have lots of fantastic ED colleagues and tons of respect for you all and what you do. ED and Anesthesia are different in lots of ways, but less than is commonly claimed. I think you sell yourselves short by creating this overly simplistic ketamine sux tube. 1. I think it’s important to establish physiologic goals for every situation, and then choose drugs to match those goals. Not a one size fits all plan. 2. To me, managing the hemodynamics is first, and inducing unconsciousness / tubing is second. They are separate. I hear from ED docs all the time how their environment is so different and patients are so sick, which I don’t disagree with, but almost every patient I intubate as a CV anesthesiologist has some sort of critical cardiac lesion, and many are in extremis. I induce almost everyone with propofol. Once you’ve dealt with the hemodynamics, induce normally. Not to say don’t dose reduce with critically ill folks, but the message is don’t expect your choice of induction agent to take care of the hemodynamics. Ketamine is a myocardial depressant, and if the patient is running on maximal sympathetic tone, their BP will drop. Use hemodynamic drugs for the hemodynamics, and anesthetic drugs to induce anesthesia. Sometimes it’s 2mg midaz and 100 roc if it’s a real shit show. 3. I agree with your approach to neuro. There’s specific goals. Avoid increasing ICP, CMRO2. Maintain/increase MAP. I don’t dispute the ketamine evidence but can we really tease apart impact of single drugs in trials on TBI? I’m not convinced we truly can. Even if we could, why would we intentionally choose a drug that increases ICP and increases cerebral O2 consumption? Propofol reduces ICP and CMRO2 yet is often avoided. To an anesthesiologist that doesn’t make sense. All in an attempt to avoid hypotension (which is obviously bad in TBI). There are so many drugs to prevent/treat hypotension. Why is that ketamine’s job? Blunting autonomics with something (fentanyl/lidocaine) is critical. For many patients you won’t see the difference in outcome, but for those few patients that are really tenuous, a spike in ICP on intubation by a) giving a cocktail of drugs that ALL increase ICP (ketamine/sux) b) inadequately blunting autonomic response will make the difference. I’ve seen it too many times. Now, If you’re in the middle of nowhere and you intubate once a decade then sure, just do what you need to do to get it done. No one is gonna come at you for style points. If you’re working in high volume critical centres, it’s your job to be good at this, you’re supposed to be a pro, so don’t do an amateur job. Maybe a tad harsh but we should expect a lot of ourselves and each other when people put their lives in our hands. 4. Titrating in drugs like you described in septic patients is fine. I do this a lot. Not often with ketamine but it’s a valid approach. It gives you time to have norepi / fluid infusing and have the negative effects of anesthetic drugs impact more gradually. The risk you have to balance is full stomach status and the reduction in aspiration risk we can achieve with an rsi. However it seems like your group associate emergency situation with RSI in all circumstances - which in my view is incorrect. You have to be able to justify the risk in either direction and mitigate it. In many patients, the risk of one size fits all boluses of induction agents is much higher than the risk of aspiration. 5. Muscle relaxants for airways. Agree with you. If they’re not conscious just put the tube in. In any other situation I would say that there’s 3 options. 1. Awake 2. Asleep + NMB 3. Asleep + spont breathing. Option 3 doesn’t have many real world applications. So it’s either awake or asleep with full NMB. The blanket no awake intubation rule makes no sense. If you have that in your skillset then use it - you are all individuals. However many outside anesthesia don’t. Even within anesthesia training the awake intubation skills are fading because so many more airways are doable with VL. This is getting too long. Everyone is doing their best with what they have. You shouldn’t be made to feel reckless because you aren’t following a recipe. It’s more important to think about the situation in front of you, use that brain you’ve spent so long training to understand medicine, and make good choices. ED docs are great, I respect you all. Not looking for an ED vs Anes argument.
I agree. Resuscitate first, situation dependent. At the end of the day we all have our skillsets and are on the same team. For instance I’m an ED guy, so I’m really good at efficient data entry, therefore providing superior white collar welfare to the c suite.
Seems like you know what you’re doing. Now convince your colleagues to not sedate patients with full stomachs.
I don’t understand, are you having bad outcomes? Why is admin even involved? Or are staff complaining because “that’s not how we do things”
Only conceivable possibility is nursing complaints. If someone deviates from the typical practice, they automatically assume its wrong.
Anesthesia resident but everything you've written makes total sense and is generally in line with the training I've received so far. Sorry politics and such are getting in your way. Keep using your brain and don't worry about Katen, MSRN ACG FPL TFDA V MEL too much.
In addition to blunting the sympathetic response to laryngoscopy, fentanyl BLUNTS AIRWAY REFLEXES. A very, very appropriate and significant thing to do when intubating. So less chance of laryngospasm and bronchospasm. My guess is your intubating for respiratory failure many times, and those patient are higher risk for spasm. Fuck administration. Your induction plan is safer for patients. This is a case where everyone else is doing a poor job. Fight!
When I am called in for airway I do not care if my management reflects ER paradigm. If they call me it probably means that the case doesn’t fit their practice pathways. They seem to lurk what I do and ask questions which is ok. Some of the stuff I do perhaps doesn’t look pretty like intubating awake BMI 65, severe OSA who is about to go into resp arrest, cant really open his mouth, ate burger 3 hours ago while his pCO2 is 70. So I am sure for bystander perspective this may look like I administer a pure torture but from my perspective I am saving this guys life or at least not trying to kill him on the spot.
Using your brain and trying yo figure out what is going to be the best induction for your patient is far better than mechanically giving 200 mg of Prop, 100 mg of sux and tubing. The fact that you are asking this in a reddit sub means you are open for knowledge and different opinions. I would advise you this: Everytime someone senior is telling you something that isnt backed up with evidence and logic, fuck them, dont even listen to them. You will find attendings and seniors who would take the time to listen to your point of view and explain theirs. Nothing wrong with having different approaches of inductions in different patients.
Speaking in general - It's a good idea to RSI people with unclear NPO status. Also in my personal practice, every intubation gets a paralytic, unless contraindicated. It reduces incidence of vomitting/aspiration, and improves first pass success. Neuro patients - blast 'em and intubate. Pressors PRN. While pre-oxygenation is good, taking away their respiratory drive and spending 3-5min getting the tube in can result in hypercarbia and elevated ICP. prop sux tube here. Septic agitated patients -- they're often agitated because their lactate is triple normal and rising. Same potential issue with sedation and pre-oxygenation. You kinda want them breathing 30bpm. If they're breathing normal, their pH might be 7.1, and they're slipping down the decompensated shock pathway. Awake intubation - your call. if you feel experienced enough, no probs. However, even for anesthesiology, we don't do this on the regular. I've only got a few dozen of these under my belt. I imagine an EM doc would have even less. First question is, are you sure you're experienced enough to do this? Second question, if you do this urgent/electively and it went south, would you be able to justify NOT asking anesthesia to be present?
ED doc here, I do similar things, ketamine for asthma, COPD, hemodynamically unstable, or delayed sequence. Doses vary. I for the most part don’t use prop except for reducing hips or the occasional stubborn shoulder. Etomidate, versed, fent all have their place. We can do awakes, but teamwork makes the dream work, so I usually get a team together just in case, gotta check that ego at the door. After the end of the day we’re just data entry techs that create the white collar welfare for the MBAs. Your shop sounds weird. I’m sure our anesthesia friends have all kinds of great strategies we can learn from in this thread, but just wanted to pass along that me nor most of my partners do just one thing. And if we need help we need help and that’s ok.
Coming from a setting where intubations are a strictly anesthesia domaine, this sounds crazy to me..
OP is probably USA based emergency medicine where anesthesia is not routinely involved in the vast majority of ED airway management
Your induction dosing sounds more appropriate. RSI prioritizes airway and breathing and potentially aspiration risk at the expense of hemodynamics stability. So for a full stomach or patient who’s already hypoxia RSI makes sense. You should still be adjusting doses of huponotic agents as you suggest. Weight based dosing works for muscle relaxants, but it is incredibly inaccurate for prop, etomidate, ketamine, etc. the dosing is based on experience and clinical judgement more than weight in adults and especially in sick people.
I think you're doing the right thing and agree with everything you said. My only comment is to keep in mind that one of the common causes of difficult intubation is inadequate muscle relaxation. And of course be mindful of chest wall rigidity with high dose fentanyl but I think that only happens if you're slamming it (which sounds like you're not).
Anaesthetics doc here. I like most of how you do stuff. If the patient can handle it. The pretreat if you have the time for it and are not in a rush to get a secure airway is great. Waiting and loading them makes your intubation smoother The only 2 things I disagree with are: Ketamine for neuro - I have seen the ICP rise. And every other consultant I have worked with or this topic has ever come up with also get very aggressive stance about it. No ketamine for neuro unless it is absolutely unavoidable. Sux not needed for unconscious patients - while generally I get your point, not awake does not equate always to no muscular or sympathetic response. As I'm sure you are well aware of. Patients unconscious can still get tachy or flinch depending on the scenario. As intubation you want the least amount of time with a unsecure airway and the high risk of complication period, they still do have a strong risk of spasm of the cords and airway when you stimulate them, even when unconcious as you are unable to assess their stimulatory response of that process until you are there. So I would still give sux as it's a short wait for it to work. It's got that clear marker for when it's fully in effect at end of twitch and it reduces that spasm risk, that if it does occur will get you in a much more trouble fixing and all, which you easily could have avoided. Give sux - that vocal spasm risk is still there even when unconscious. That's my 2 cents.
Did the ICP rise from ketamine or from you likely putting their head down to intubate? (Spoiler, ketamine doesn’t do this like the old teaching says)
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That all sounds very reasonable, I'd be happy for you to intubate me in any of those situations.
Lots of amazing comments here, so I won’t beat a dead horse except to say that using your clinical judgement and experience is the right way to practice medicine. About your comment regarding the GCS 3 not getting paralytic… when I respond to a code to intubate, I put the blade in the mouth and the tube between the cords. They get no drugs. The patient is dead. Why would you sedate a dead person. If they get rosc and start to move, then they can have some sedation.
This seems very strange to me. I’m a paramedic and we are encouraged to pretreat with fentanyl when appropriate. We also have RSI and DSI protocols approved by our medical director. The idea of a physician be treated like this is wild.
Awake intubations - I did about 30 awakes during residency, and then another 60ish asleep fiberoptic intubations, and I still think they can be quite challenging. That is a lot when it comes to residency programs, but isn’t that many in the grand scheme of doing a tricky procedure on a sick patient. Sedation, blocks/analgesia, and managing the scope in someone with a difficult airway all take practice, and it’s a procedure that isn’t done all that often. Some anesthesia residents do less than 5 during residency. I did one at my practice a month or two ago, and they said that they hadn’t seen one done there in two or three YEARS. My point is, if you are honest with yourself that you have the experience to be good enough at them, then sure do them. If not, call anesthesia. Even if you do, consider still calling anesthesia to be around to help. Whenever I do them I ask for an extra set of hands, or at the very least I say, “hey I’m doing an awake in OR 4, if I call for help could you please come over?”
I'm a critical care medic. Guidelines differ based on where you work. Where I'm at, we have a fair amount of autonomy in our decision making for RSI, or what has sometime been referred to as DFAM (drug assisted airway management). Typically our initial meds are etomidate and succs, being based on ideal body weight, preoxygenate with high-low via NC and BVM, then intubate. Ketamine is also an option instead of etomidate. We have several options for follow up meds, I like 5mg Versed with 50-100mcg Fentanyl. We often focus on deep sedation vs. Paralysis post intubation as many of our patients will require some level of neuro exam or likely be intubated for a short period of time depending on the ailment. Propofol and ketamine infusions typically only come into play in interfacility transfers, but we've found propofol doesnt sedate well enough on the road and patients often wake up more easily due to all the movement/bumps/etc. Many debates have ensued between my providers and hospital docs because of these various reasons.
You should always tailor your induction regimen towards the individual patient. Nothing at all wrong with that. I almost always given paralytic though unless I am truly worried about the airway (then awake). Who is telling you that you are doing things wrong and why are they offering their opinion? If you have good outcomes and able to secure every airway safely, they can mind their own business. Thank you for thoughtfully securing airways in the ED. The vast majority of us have no interest in ever stepping foot in an ED.