etomidate

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migm

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Being forced to use etomidate at times. Not a medication I really used very often in training. For the hypotensive/hypovolemic trauma/sepsis pt, talk to me about dosing. Seems like etomidate does not require dose reduction in these instances, and may even benefit from dose increase to get reliable induction?

thanks for chiming in with your experience, just trying to be prepared for the inevitable even though it's not my first choice agent, to say the least
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Was just cruising by when I saw this topic.

migm said:
Being forced to use etomidate at times. Not a medication I really used very often in training. For the hypotensive/hypovolemic trauma/sepsis pt, talk to me about dosing. Seems like etomidate does not require dose reduction in these instances, and may even benefit from dose increase to get reliable induction?

thanks for chiming in with your experience, just trying to be prepared for the inevitable even though it's not my first choice agent, to say the least
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Maybe not, but every code cart I've ever used has always had etomidate in it. Unlike your other induction agent options - propofol, ketamine, even opiates/benzos - it is highly unlikely to be considered a controlled substance, which means it can readily be obtained and stored in easy-to-get locations (like a crash cart). Get some comfort using it, because outside of the ED it's probably going to be your only option especially on the med-surg floor.

I usually give 0.2-0.3 mg/kg as an induction dose (don't really go below 8 mg or above 20 mg), and as you allude to I don't adjust it for any special situations as it doesn't have the SVR reduction propofol has. Of course, you get a sick enough patient reliant on their awake sympathetic drive you'll see hypotension for sure - but I'm not sure giving "less" etomidate would attenuate how much hypotension you'd see.

Anyways, back to the anethesia forum for me!
 
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migm said:
Being forced to use etomidate at times. Not a medication I really used very often in training. For the hypotensive/hypovolemic trauma/sepsis pt, talk to me about dosing. Seems like etomidate does not require dose reduction in these instances, and may even benefit from dose increase to get reliable induction?

thanks for chiming in with your experience, just trying to be prepared for the inevitable even though it's not my first choice agent, to say the least
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This is interesting. I'm 4 years out of training and grew up with Etomidate, and still use a lot of it. Started using Ketamine for trauma towards the end of training but still used Etomidate for medical intubations. What were you using in training?

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migm said:
Being forced to use etomidate at times. Not a medication I really used very often in training. For the hypotensive/hypovolemic trauma/sepsis pt, talk to me about dosing. Seems like etomidate does not require dose reduction in these instances, and may even benefit from dose increase to get reliable induction?

thanks for chiming in with your experience, just trying to be prepared for the inevitable even though it's not my first choice agent, to say the least
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Did you do an EM residency or are you coming from another speciality? Etomidate is bread and butter EM. I simplify and use two doses: 20 for a small person, 30 for almost everyone else. But officially it’s 0.3-0.4 mg/kg.
 
Etomidate does not have any intrinsic negative hemodynamics effects. If you have hypotension after using it, it is likely the result of shutting down the patient's sympathetic drive. If they are depending on that sympathetic tone, hypotension will come with virtually every induction agent
 
As I recall from residency, I gave just about every adult I every met 20mg etomidate and had no issues inducing them. I did get some hypotension though.

I'm a bit more cultured now, and do like ketamine for the truly hypotensive I haven't really full resuscitated prior to intubation.

That said, as opposed to residency, I do tend to delay the intubation for 10-15minutes to get 2L NS and levophed hanging when possible... just works out much better for all of us.

Now I use 20mg for normal adults, and 10mg for the tiny, elderly, already nearly-comatose don't really even need induction septi-bombs and strokes from SNFs as a rule of thumb.
 
engineeredout said:
Etomidate does not have any intrinsic negative hemodynamics effects. If you have hypotension after using it, it is likely the result of shutting down the patient's sympathetic drive. If they are depending on that sympathetic tone, hypotension will come with virtually every induction agent
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Agreed.

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where did you train that you didn't get exposed to etomidate? Thats the standard at most shops unless they are letting the residents play around with versed, ketamine, propofol, etc. The best thing about etomidate is the nurses are comfortable with it. I find that you get a lot more dosing questions when using other agents, not something you want to waste brainpower on during an emergent intubation.
 
Is etomidate out of favor now? Use it all the time. 5 might be enough for a cardioversion, but I typically don't give less than 20 to intubate. The only issue I know with using it involves septic patients who later end up with adrenal insufficiency. Is there some other reason not to use it?
 
Jlaw said:
where did you train that you didn't get exposed to etomidate? Thats the standard at most shops unless they are letting the residents play around with versed, ketamine, propofol, etc. The best thing about etomidate is the nurses are comfortable with it. I find that you get a lot more dosing questions when using other agents, not something you want to waste brainpower on during an emergent intubation.
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Exactly, which is why I use my simple 20 for a small patient, 30 for a regular person. Never had any issues, and don't need to waste brain cells on it... Bottom line: I love Etomidate.
 
The White Coat Investor said:
Is etomidate out of favor now? Use it all the time. 5 might be enough for a cardioversion, but I typically don't give less than 20 to intubate. The only issue I know with using it involves septic patients who later end up with adrenal insufficiency. Is there some other reason not to use it?
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Vomidate? Then there's the myoclonus. The anesthesia guys REALLY don't like it. I just looked at a thread there from 3 years ago. Even then, they were crucifying it.

If it's all you got, then that's it. But, when the guys who have opportunity to use it a lot more than we do choose not to use it, that should give you pause.
 
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Apollyon said:
Vomidate? Then there's the myoclonus. The anesthesia guys REALLY don't like it. I just looked at a thread there from 3 years ago. Even then, they were crucifying it.

If it's all you got, then that's it. But, when the guys who have opportunity to use it a lot more than we do choose not to use it, that should give you pause.
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How would vomiting or myoclonus affect us in the ER? When I'm tubing someone, I give them sedation meds and put them under... Just saying, I've never had an issue with Etomidate despite using it all the time.... Your thoughts?
 
Angry Birds said:
How would vomiting or myoclonus affect us in the ER? When I'm tubing someone, I give them sedation meds and put them under... Just saying, I've never had an issue with Etomidate despite using it all the time.... Your thoughts?
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Same here. Use etomidate and succinylcholine almost every time for rsi and never had any problems for the last 5 Years...


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When I was teaching, I would routinely tell residents that the drug they use all the time is now gone. Not to be a dick, but to broaden their toolbox. Also, in the current climate of frequent shortages (etomidate being one of them), it's always nice to know the drugs you need right now vs the ones you have time to look up.

But yes, etomidate is fine. Any pt with poor perfusion needs higher doses of everything because they're not perfusing well. I generally recommend ketamine in those people but many hospitals still don't allow it for EPs.
 
Angry Birds said:
How would vomiting or myoclonus affect us in the ER? When I'm tubing someone, I give them sedation meds and put them under... Just saying, I've never had an issue with Etomidate despite using it all the time.... Your thoughts?
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I've seen the myoclonus and the vomiting. You state the "fallacy of anecdote" - "I've never seen it, so it must not exist". I don't know how much "all the time" is, but I'll bet the opportunities for the anesthesiologists are more prevalent than yours.

But, still, as I say, if that's what you have, that's what you use. You do you. But, if I was a suburban cop, I would listen to the city guys, and follow their lead, were I given an option. But, you do you. That's what you do best.
 
Apollyon said:
I've seen the myoclonus and the vomiting. You state the "fallacy of anecdote" - "I've never seen it, so it must not exist". I don't know how much "all the time" is, but I'll bet the opportunities for the anesthesiologists are more prevalent than yours.

But, still, as I say, if that's what you have, that's what you use. You do you. But, if I was a suburban cop, I would listen to the city guys, and follow their lead, were I given an option. But, you do you. That's what you do best.
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If I were a suburban cop, who dabbled in city issues, I'd listen to the city guys. But when it comes to suburban policing, the issues are different, and the city guys may not be the experts you're looking for. Different environment, different knowledge base. The pay off for using etomidate in the majority of OR cases (known patient, with a known history, and a pre-op plan in place) is significantly less than in the ED.
 
Apollyon said:
I've seen the myoclonus and the vomiting. You state the "fallacy of anecdote" - "I've never seen it, so it must not exist". I don't know how much "all the time" is, but I'll bet the opportunities for the anesthesiologists are more prevalent than yours.

But, still, as I say, if that's what you have, that's what you use. You do you. But, if I was a suburban cop, I would listen to the city guys, and follow their lead, were I given an option. But, you do you. That's what you do best.
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Are you EM or anesthesia?
 
The analogy to city police is worse /bigger felony crimes. Suburban guys (fortunately) don't have to deal with as many gangs, murders, rapes, or gun violence. Just like that, the number of RSIs in the ED is dwarfed by those in the OR. When the big crimes come to suburbia, the urban knowledge can be valuable.

But, again, I'm not trying to manipulate anyone.
 
Angry Birds said:
Are you EM or anesthesia?
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Dude, I've been on this forum more than twice as long as you, I believe I have about 6 times as many posts, and have clearly commented on my EM residency, jobs, and other topics.

It's some case of loss of memory by you for times when we've directly interacted, simple non intersection between what I've posted and what you've read, a glaring lack of any providence of anything I've ever posted (that is, I'm insipid, and what I do post sucks), and you using some sort of literary technique where you know the answer, but ask the question anyways.

I say this, because, if I said, "you know I'm EM", that could mean you might not know.

But, again - you've never seen myoclonus directly after RSI? I can't say "you will", but it does happen. It is similar for the vomiting.
 
Apollyon said:
Dude, I've been on this forum more than twice as long as you, I believe I have about 6 times as many posts, and have clearly commented on my EM residency, jobs, and other topics.

It's some case of loss of memory by you for times when we've directly interacted, simple non intersection between what I've posted and what you've read, a glaring lack of any providence of anything I've ever posted (that is, I'm insipid, and what I do post sucks), and you using some sort of literary technique where you know the answer, but ask the question anyways.

I say this, because, if I said, "you know I'm EM", that could mean you might not know.

But, again - you've never seen myoclonus directly after RSI? I can't say "you will", but it does happen. It is similar for the vomiting.
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Lol dude I’ve seen you post and thought you were EM but then I also know some people post across forums. Just making sure. Wasn’t some slick rhetorical move or anything. I certainly can’t be expected to remember your training and stuff. Also I’m on my phone while between sets at the gym haha.

My follow up question is: how does myoclonus affect me as the EM physician in an intubated and sedated patient?

I’m not trying to be an ass. I’m legit asking to learn.
 
Angry Birds said:
Lol dude I’ve seen you post and thought you were EM but then I also know some people post across forums. Just making sure. Wasn’t some slick rhetorical move or anything. I certainly can’t be expected to remember your training and stuff. Also I’m on my phone while between sets at the gym haha.

My follow up question is: how does myoclonus affect me as the EM physician in an intubated and sedated patient?

I’m not trying to be an ass. I’m legit asking to learn.
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The myoclonus occurs before the paralysis. That's the thing. Once the paralytic is on board, the chemical emetogenesis and the myoclonus literally can't be seen.
 
Etomidate is a great drug. The adrenal suppression thing is overblown. Anesthesia doesn’t like it because it’s not propofol. It’s relatively hemodynamically neutral, but I dose reduce in someone who is truly hypotensive - usually about a half dose. As a rule of thumb, with a patient in shock (and some mental status), I’ll increase paralytic by 50% and cut my induction dose by 50%.

Yes, you have vomiting and myoclonus, which is why I don’t love it for procedural sedation, but followed by succs or roc, it’s fine.
 
Apollyon, what is your first line induction agent, since it appears to not be etomidate?
 
goodoldalky said:
Apollyon, what is your first line induction agent, since it appears to not be etomidate?
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What did I say? If that's what you got, that's what you use. That's what I said. Etomidate is what I have. I HAVE to use it. Don't like it, but, it is what it is.

That's what's in the kit. If I can convince a nurse, I can get them to pull the propofol. However, that is uncommon.
 
I've not attempted propofol for intubation in the ED, but I can see why it would be a good choice in some circumstances. Seems like a lot of the patient's I intubate are not exactly stable though, so I end up using etomidate or ketamine. I guess I'm lucky because we have everything available here.
 
(1) I have used propofol to tube in a few times-- either responding to an ICU where it is already hanging there (as opposed to waiting minutes for etomidate to be found) or in the ED if they have a super high BP and I'm putting them on propofol for sedation anyway.

It's nice and smooth, but it has significant hemodynamic effects in a large cohort of the types of patients we're intubation.

(2) As well, i have CERTAINLY scene myoclonus from etomidate. I've used it in the 10mg dose for brief sedation in various locales where I didn't have ketamine / propofol. It works fine for cardio version, chest tubes, huge abscesses, quick reductions (like say frx/dislocated ankle you know will pop right back over). But when you have propofol and are facile with its use... lets just say I do etomidate sedation maybe once a year currently....
 
AdmiralChz said:
Was just cruising by when I saw this topic.



Maybe not, but every code cart I've ever used has always had etomidate in it. Unlike your other induction agent options - propofol, ketamine, even opiates/benzos - it is highly unlikely to be considered a controlled substance, which means it can readily be obtained and stored in easy-to-get locations (like a crash cart). Get some comfort using it, because outside of the ED it's probably going to be your only option especially on the med-surg floor.

I usually give 0.2-0.3 mg/kg as an induction dose (don't really go below 8 mg or above 20 mg), and as you allude to I don't adjust it for any special situations as it doesn't have the SVR reduction propofol has. Of course, you get a sick enough patient reliant on their awake sympathetic drive you'll see hypotension for sure - but I'm not sure giving "less" etomidate would attenuate how much hypotension you'd see.

Anyways, back to the anethesia forum for me!
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thank you sir or madam

alphaholic06 said:
This is interesting. I'm 4 years out of training and grew up with Etomidate, and still use a lot of it. Started using Ketamine for trauma towards the end of training but still used Etomidate for medical intubations. What were you using in training?

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Angry Birds said:
Did you do an EM residency or are you coming from another speciality? Etomidate is bread and butter EM. I simplify and use two doses: 20 for a small person, 30 for almost everyone else. But officially it’s 0.3-0.4 mg/kg.
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I'm EM trained, graduated in the last 5 years, board certified in same, from a program you would recognize immediately. We didn't use etomidate very much and thus my n for intubation in patients with altered hemodynamics is low. Hence my question. Ketamine was quite the preferred agent, much like etomidate once was.

TooMuchResearch said:
I reduce dosing in many unstable patients. I also preferentially use ketamine, which I also dose reduce. Scott Weingart has a name for reducing the dose, but I don't recall what it is.
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Jlaw said:
where did you train that you didn't get exposed to etomidate? Thats the standard at most shops unless they are letting the residents play around with versed, ketamine, propofol, etc. The best thing about etomidate is the nurses are comfortable with it. I find that you get a lot more dosing questions when using other agents, not something you want to waste brainpower on during an emergent intubation.
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I don't really want to say where I trained, but its a well known and regarded residency. I was certainly exposed to etomidate, but I used it approximately for 1 in 15 or 20 intubations.

The White Coat Investor said:
Is etomidate out of favor now? Use it all the time. 5 might be enough for a cardioversion, but I typically don't give less than 20 to intubate. The only issue I know with using it involves septic patients who later end up with adrenal insufficiency. Is there some other reason not to use it?
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Ketamine is all the rage, man. All the kids are doing it.

Dr.McNinja said:
//But yes, etomidate is fine. Any pt with poor perfusion needs higher doses of everything because they're not perfusing well. I generally recommend ketamine in those people but many hospitals still don't allow it for EPs.
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when I trained there really weren't drug shortages like this. Anyway, ketamine was the go to. Propofol and etomidate were def. second rung.

TimesNewRoman said:
Etomidate is a great drug. The adrenal suppression thing is overblown. Anesthesia doesn’t like it because it’s not propofol. It’s relatively hemodynamically neutral, but I dose reduce in someone who is truly hypotensive - usually about a half dose. As a rule of thumb, with a patient in shock (and some mental status), I’ll increase paralytic by 50% and cut my induction dose by 50%. ...
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There is a disagreement among the responders as to what (see above), if any and what kind of dose adjustment is required in the scenario given. I certainly do adjust my ketamine dosing in shocky patients (decrease) though I'm not sure what data there is for same.
 
Apollyon said:
I've seen the myoclonus and the vomiting. You state the "fallacy of anecdote" - "I've never seen it, so it must not exist". I don't know how much "all the time" is, but I'll bet the opportunities for the anesthesiologists are more prevalent than yours.

But, still, as I say, if that's what you have, that's what you use. You do you. But, if I was a suburban cop, I would listen to the city guys, and follow their lead, were I given an option. But, you do you. That's what you do best.
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When are you seeing the vomiting? My understanding of the literature is that the concern is related to postop nausea/vomiting, e.g. a long time after you push it. If I'm giving etomidate for procedural sedation (which I don't do) I could see this as a problem. If I'm doing this for intubation... who cares? They're going to be paralyzed and vented momentarily. Just curious if you're seeing issues with it in the setting of RSI.
 
TimesNewRoman said:
Etomidate is a great drug. The adrenal suppression thing is overblown. Anesthesia doesn’t like it because it’s not propofol. It’s relatively hemodynamically neutral, but I dose reduce in someone who is truly hypotensive - usually about a half dose. As a rule of thumb, with a patient in shock (and some mental status), I’ll increase paralytic by 50% and cut my induction dose by 50%.

Yes, you have vomiting and myoclonus, which is why I don’t love it for procedural sedation, but followed by succs or roc, it’s fine.
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This is my rule of thumb also.
 
Apollyon said:
The myoclonus occurs before the paralysis. That's the thing. Once the paralytic is on board, the chemical emetogenesis and the myoclonus literally can't be seen.
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Ok so this is why I don’t think it’s very important. I’m slamming a paralytic in right after the etomidate. So what are the chances that I’d have to deal with myoclonus or vomiting?
 
migm said:
There is a disagreement among the responders as to what (see above), if any and what kind of dose adjustment is required in the scenario given. I certainly do adjust my ketamine dosing in shocky patients (decrease) though I'm not sure what data there is for same.
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Just because there isn’t agreement doesn’t mean that there isn’t a right answer. There’s not data, but I can tell you that the higher the dose of sedative, the more hemodynamical effect. I can also tell you that I’ve never had any recall using this method. Seems simple enough.

Plus, if someone is ever super unstable, just go light and just get the tube in to make sure you keep them alive, then give a couple of versed once tubed for retrograde amnesia.
 
Apollyon said:
The myoclonus occurs before the paralysis. That's the thing. Once the paralytic is on board, the chemical emetogenesis and the myoclonus literally can't be seen.
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I’ve never seen myoclonus in when etomidate is followed by a paralytic. I’ve only ever seen succs related fasiculations.
 
Apollyon said:
Vomidate? Then there's the myoclonus. The anesthesia guys REALLY don't like it. I just looked at a thread there from 3 years ago. Even then, they were crucifying it.

If it's all you got, then that's it. But, when the guys who have opportunity to use it a lot more than we do choose not to use it, that should give you pause.
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Anesthesia doesn't like it because of the adrenal suppression nonsense that they still believe.
 
Heh kind of a strange post, is your base certification in EM? The reason I ask is in residency we used etomidate for probably 90% of intubations, this also appears to be true at most academic institutions I have observed as a visiting student, visiting resident, and clinical staff attending. Etomidate is a near "perfect" RSI drug for the ER setting where fast onset, fast offset, and "hemodynamically neutrality" are very important features for intubating the undifferentiated sick patient who is at risk for peri-intubation hypotension.

That being said to answer your question, the "RSI dose" for etomidate is technically 0.3mg/kg. One institution I work at the RNs reflexively draw up 30mg for an adult and another institution they draw up 20mg. Both seem to work well. I do not frequently use etomidate in children mostly out of habit (the pediatricians that trained me shunned etomidate, propofol, and succinylcholine). It can be used for procedural sedation as well with a dose of 0.1-0.15mg/kg with option to re-bolus so functionally about 5-10mg x2. I do not love it for procedural sedation because there is risk for apnea and myoclonus which is an annoying side effect when trying to do a reduction. As other posters have noted, the paralytic of an RSI prevents any myoclonus during RSI with etomidate.

the 10% of intubations I do not use etomidate in are patients who are already hypotensive or those who I am doing a "delay sequence" (a la Scott Weingart) to maximize preoxygenation with BiPAP in a combative hypoxic patient; in which case i use ketamine 2mg/kg. Alternatively, you can use lower dose etomidate (and higher dose paralytic) for hypotensive intubations especially if the patient is already fairly obtunded/altered from their shock state, say 10-15mg.

I have never used veresed, propofol, or thiopental for intubations in the ER.
 
BoardingDoc said:
When are you seeing the vomiting? My understanding of the literature is that the concern is related to postop nausea/vomiting, e.g. a long time after you push it. If I'm giving etomidate for procedural sedation (which I don't do) I could see this as a problem. If I'm doing this for intubation... who cares? They're going to be paralyzed and vented momentarily. Just curious if you're seeing issues with it in the setting of RSI.
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For elective procedural sedation I almost always pre-medicate with zofran 8mg IV like 15 minutes before sedative.
 
Brigade4Radiant said:
Ketamine has given me more vomiting than etomidate.
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I always give kids Zofran before the ketamine. Haven't really had any issues with adults.

I've seen some good pre-vomit retching in adults post etomidate, but infrequent enough that I don't always give Zofran first.
 
engineeredout said:
Anesthesia doesn't like it because of the adrenal suppression nonsense that they still believe.
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What
It is very associated with continued infusions and definitely exists. There are also trials and case studies that suggest that it also manifests after a single dose to the point where annane had to exclude patients who received it in his 2002 study for steroids in septic shock
 
I have seen papers supporting the notion that adrenal suppression can occur with 1 dose of etomidate, but the outcomes measured weren't the ones that mattered.

In other words, there may be measurable adrenal suppression, but it did NOT have any meaningful impact on patient outcomes.

If anybody has new or better data to suggest otherwise, please share it so we can all learn.
 
Psai said:
What
It is very associated with continued infusions and definitely exists. There are also trials and case studies that suggest that it also manifests after a single dose to the point where annane had to exclude patients who received it in his 2002 study for steroids in septic shock
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Yes, it influences your cort stim test but doesn’t influence patient-centered outcomes. Continuous infusion etomidate certainly does have strong adrenal suppressing effects, but that’s very different from giving someone 10-30mgs X1.
 
I don't think it makes a major difference and anything that happens can be fixed with a short course of pressors at the most. That is different from trying to call out another field for "believing in nonsense" for something that's a real, well documented phenomenon.
 
Psai said:
I don't think it makes a major difference and anything that happens can be fixed with a short course of pressors at the most. That is different from trying to call out another field for "believing in nonsense" for something that's a real, well documented phenomenon.
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No. It’s nonsense to think that a single dose of etomidate causes problems.
 
Psai said:
What
It is very associated with continued infusions and definitely exists. There are also trials and case studies that suggest that it also manifests after a single dose to the point where annane had to exclude patients who received it in his 2002 study for steroids in septic shock
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Psai said:
I don't think it makes a major difference and anything that happens can be fixed with a short course of pressors at the most. That is different from trying to call out another field for "believing in nonsense" for something that's a real, well documented phenomenon.
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Right, associated with continuous infusions, not one time usage for RSI, and even in the cases where it has been detected, it is, for now, a lab abnormality which has never been tied to clinically meaningful outcomes. So yes I will call out people who come in and say I can't use a one time dose of etomidate due to adrenal suppression, but then will give my septic patient a big old slug of propofol and watch their blood pressure crap out.
 
 
Psai said:
Single induction dose of etomidate versus other induction agents for endotracheal intubation in critically ill patients. - PubMed - NCBI
The Effects of Single-Dose Etomidate Versus Propofol on Cortisol Levels in Pediatric Patients Undergoing Urologic Surgery: A Randomized Controlled ... - PubMed - NCBI
Etomidate is associated with mortality and adrenal insufficiency in sepsis: a meta-analysis*. - PubMed - NCBI
Adrenal suppression following a single dose of etomidate for rapid sequence induction: a prospective randomized study. - PubMed - NCBI

You're welcome.
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I’m aware of all of this and its garbage data. One of which is a study of pediatrics, an entirely different patient population and something I wasn’t speaking to (although admitted I wasn’t clear in this). The others essentially show exactly what I just said: change in adrenal studies. Some suggest mortality but are significantly methodologically flawed. The best literature to date shows no patient centered outcome changes.

Edited for typo.
 
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Psai said:
Single induction dose of etomidate versus other induction agents for endotracheal intubation in critically ill patients. - PubMed - NCBI
The Effects of Single-Dose Etomidate Versus Propofol on Cortisol Levels in Pediatric Patients Undergoing Urologic Surgery: A Randomized Controlled ... - PubMed - NCBI
Etomidate is associated with mortality and adrenal insufficiency in sepsis: a meta-analysis*. - PubMed - NCBI
Adrenal suppression following a single dose of etomidate for rapid sequence induction: a prospective randomized study. - PubMed - NCBI

You're welcome.
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Here’s the largest (I believe) systematic review on the topic - we’ll over 5x larger than what you cited:
Single-dose etomidate does not increase mortality in patients with sepsis: a systematic review and meta-analysis of randomized controlled trials and ... - PubMed - NCBI
Regardless, most everything showing harm is a post-hoc analysis.

The two big prospective RCTs I’m aware of show no difference in mortality:

Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: a multicentre randomised controlled trial. - PubMed - NCBI

http://www.annemergmed.com/article/S0196-0644(16)30467-X/abstract

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