etomidate

[Psai]

The point of contention was whether or not etomidate induces adrenal suppression.

Your systematic review states: "Eight of the included studies provided data for adrenal insufficiency.16, 18, 19, 21, 23, 24, 27, 31 Single-dose etomidate increased the risk of adrenal insufficiency in patients with sepsis (RR, 1.42; 95% CI, 1.22-1.64; P < .00001) (Fig 3)."

We're only beginning to understand the long term effects that icu stays have on patients. Why use a drug that may cause problems over others that may not? I've seen etomidate cause emesis and near aspiration in a patient. Timely intervention occurred prior to a poor outcome and no negative patient centered outcomes were recorded. I prefer to avoid it altogether.

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[littlejuan]

The point of contention was whether or not etomidate induces adrenal suppression.

Your systematic review states: "Eight of the included studies provided data for adrenal insufficiency.16, 18, 19, 21, 23, 24, 27, 31 Single-dose etomidate increased the risk of adrenal insufficiency in patients with sepsis (RR, 1.42; 95% CI, 1.22-1.64; P < .00001) (Fig 3)."

We're only beginning to understand the long term effects that icu stays have on patients. Why use a drug that may cause problems over others that may not? I've seen etomidate cause emesis and near aspiration in a patient. Timely intervention occurred prior to a poor outcome and no negative patient centered outcomes were recorded. I prefer to avoid it altogether.

Do you suggest propofol for RSI in the septic hypotensive patient?

I’ve also seen a lot of things go bad with all kinds of drugs. Severe bronchospasms after adenosine use for instance. Anecdotes aren’t really the best way to go about medicinal treatment and interventions.

 

[SpacemanSpifff]

The point of contention was whether or not etomidate induces adrenal suppression.

Your systematic review states: "Eight of the included studies provided data for adrenal insufficiency.16, 18, 19, 21, 23, 24, 27, 31 Single-dose etomidate increased the risk of adrenal insufficiency in patients with sepsis (RR, 1.42; 95% CI, 1.22-1.64; P < .00001) (Fig 3)."

We're only beginning to understand the long term effects that icu stays have on patients. Why use a drug that may cause problems over others that may not? I've seen etomidate cause emesis and near aspiration in a patient. Timely intervention occurred prior to a poor outcome and no negative patient centered outcomes were recorded. I prefer to avoid it altogether.

Every drug has its own set of problems. One of the most common probelms I want to avoid in patients we intubate in the ED? Hypotension. Etomidate or ketamine it is.

 

[Psai]

So you are trading hypotension in the ed for hypotension in the icu. As long as it doesn't happen while the patient is under your care, why does it matter right?

If you need to support the pressure, then you should support the pressure.

Ketamine can cause myocardial depression and etomidate can cause hypotension.

You can use any induction agent or even none. Dose matters more than the agent.

 

[deleted547339]

So you are trading hypotension in the ed for hypotension in the icu. As long as it doesn't happen while the patient is under your care, why does it matter right?

If you need to support the pressure, then you should support the pressure.

Ketamine can cause myocardial depression and etomidate can cause hypotension.

You can use any induction agent or even none. Dose matters more than the agent.

No, we’re trading hypotension in the ER for an abnormal cort stim test.

 

[The Physician Philosopher]

Anesthesia doesn't like it because of the adrenal suppression nonsense that they still believe.

We don't like it in anesthesia for a few reasons. Some of them valid. Some not so much, but I definitely use it in my critically ill patients that aren't going to tolerate a propofol induction.

1. There was a bad study done out of Cleveland Clinic that most anesthesia docs read that showed that etomidate led to an increased rate of mortality. This post would get too long to go into the reasons why it wasn't a good study. Unfortunately, it was published in a very well read anesthesia journal (Anesthesia & Analgesia) and people bought it hook, line, and sinker.
2. Myoclonus. Why use etomidate if someone is stable enough to get propofol, which is a predictable and smooth induction (Aside from pain for the patient on induction).
3. Adrenal suppression. More theoretical. I don't think most of us in anesthesia care about this and in a one-time situation as it is unlikely to be meaningful. Now if you are having a procedure done that is going to occur over and over (skin grafts, dressing changes, abdominal wash-outs/closures) etomidate is probably not the best because repeated use can certainly lead to adrenal suppression.

To answer the original question by the OP, etomidate does provide a stable induction (if the person isn't dependent on their sympathetic drive to keep their pressure up). A dose of 0.3 mg/kg is usually sufficient. Can certainly get away with much less in a critically sick patient.

 

[heavyd85]

there are many ways to skin a cat. As a cardiac anesthesiologist and intesivist I rarely (I actually only used it in residency for etc) use etomidate, but that does not mean it is a bad drug. I agree that the adrenal suppression argument is overblown in one time use (abnormal cort stim doesn't mean clinically significant adrenal suppression). I regularly induce patients with LVEF < 10% (we do lots of heart transplants) and use propofol 100% of the time and rarely have resultant hypotension. One
Must anticipate the side effects of a medication and treat appropriately (i.e. Give 64 mcg norepi, 30 mcg epi, etc with said dose). When inducing a sick patient I stick to what I know and avoid medications I rarely use. A big difference between the OR and ED is that I have all the meds I want and personally administer them. In the ed the nurses push the meds with a verbal order from the physician. It is a hell of a lot easier to say 20 of etomidate and 100 of sux. Also if a patient is NPO I can slowly titrate propofol until the patient is unconcious as I am very comfortable doing this. With etomidate this is much harder when the patient is flailing around due to myoclonus. I think it is misguided to suggest we are fools for "clinging to propofol."

 

[The Physician Philosopher]

there are many ways to skin a cat. As a cardiac anesthesiologist and intesivist I rarely (I actually only used it in residency for etc) use etomidate, but that does not mean it is a bad drug. I agree that the adrenal suppression argument is overblown in one time use (abnormal cort stim doesn't mean clinically significant adrenal suppression). I regularly induce patients with LVEF < 10% (we do lots of heart transplants) and use propofol 100% of the time and rarely have resultant hypotension. One
Must anticipate the side effects of a medication and treat appropriately (i.e. Give 64 mcg norepi, 30 mcg epi, etc with said dose). When inducing a sick patient I stick to what I know and avoid medications I rarely use. A big difference between the OR and ED is that I have all the meds I want and personally administer them. In the ed the nurses push the meds with a verbal order from the physician. It is a hell of a lot easier to say 20 of etomidate and 100 of sux. Also if a patient is NPO I can slowly titrate propofol until the patient is unconcious as I am very comfortable doing this. With etomidate this is much harder when the patient is flailing around due to myoclonus. I think it is misguided to suggest we are fools for "clinging to propofol."

The other thing here is that when I do a "cardiac induction" I load people up with a boatload of opioid (i.e. fentanyl) so that they require less of whichever induction agent I use and will tolerate the direct laryngoscopy. Also, like you said, we have time to titrate an induction versus the RSI that has to occur in the ED. No time to slowly titrate propofol with pressors in that situation.

In a lot of cases in the non-cardiac world I don't have time to let that amount of fentanyl get metabolized. I say I use propofol 98% of the time. Shoot I used methohexital to induce a patient the other day for a non-ECT case (I work in an academic center). I like to stay familiar with all of the drugs and think that there are indications for each induction drug's use.

 

[deleted547339]

there are many ways to skin a cat. As a cardiac anesthesiologist and intesivist I rarely (I actually only used it in residency for etc) use etomidate, but that does not mean it is a bad drug. I agree that the adrenal suppression argument is overblown in one time use (abnormal cort stim doesn't mean clinically significant adrenal suppression). I regularly induce patients with LVEF < 10% (we do lots of heart transplants) and use propofol 100% of the time and rarely have resultant hypotension. One
Must anticipate the side effects of a medication and treat appropriately (i.e. Give 64 mcg norepi, 30 mcg epi, etc with said dose). When inducing a sick patient I stick to what I know and avoid medications I rarely use. A big difference between the OR and ED is that I have all the meds I want and personally administer them. In the ed the nurses push the meds with a verbal order from the physician. It is a hell of a lot easier to say 20 of etomidate and 100 of sux. Also if a patient is NPO I can slowly titrate propofol until the patient is unconcious as I am very comfortable doing this. With etomidate this is much harder when the patient is flailing around due to myoclonus. I think it is misguided to suggest we are fools for "clinging to propofol."

Sorry, the “cling to propofol” thing was in jest. A lot of my buddies are anesthesiologists and I bust on them for it frequently. They induce almost everyone with prop + some quantity of vasopressor and I always jokingly remind them that they could use one drug instead of two and make things simplier. Hope there are no hard feelings - it really wasn’t meant to cause offense.

That’s interesting about you using propofol for CT anesthesia - I know that’s what our CT guys use, but my understanding is that it’s not the norm - wonder if we’re at the same place.

Anyways, I have to say I’m very impressed by your insight. Many of the anesthesiologists who I have come across lack the insight to understand the reason why we do things so differently in the ER - it’s not just a culture thing, Honestly, most all doctors don’t really understand the ER in spite of how much people interact with us (no, coming to the ER isn’t the right place to expedite the non-emergent workup for x/y/z; no, our goal isn’t to thoroughly work up all of their problems, it’s to recognize and stabilize the life and limb threats and dispo somewhere that someone else can deal with the rest; no, being late to your follow up appointment isn’t a reason to send someone the ER so you can let your office staff go home and meet them here). I know this may sound silly, but I suspect the overwhelming majority of doctors don’t really “get it” when it comes to the ER.

Back to the propofol thing, I really do think that if you told everyone who intubates that they only had one induction med chosen at random (plus appropriate analgesia and anxiolytics), you could safely intubate for the rest of your career and have outcomes no different than anyone else. E.g. if you were told you could only ever use etomidate and I was told I could only ever use ketamine, people would be fine. I think there are good reasons to use one induction med over another (I.e. I always use prop when I have a patient in status epilepticus and ketamine in status asthmaticus). I think we live in a really cool time when we have a lot of safe anesthestics for induction and knowing the medicine inside and out is probably more important than “using the right drug.” I think your using propofol for your CT patients is a perfect example of that. Everything I’ve read says to use something more hemodynamically stable with a bad heart, but an expert can safely use whatever they want and do it right when they understand and anticipate the consequences of the drugs they are giving.

That’s not to say I haven’t seen some things go really wrong (e.g. junior anesthesia resident trying to intubate a sick trauma patient with as much propofol as they would use on a healthy patient in the OR), but these are mistakes in understanding the drug, not an inherent problem in the drug. I think most ER docs are not experts in all induction drugs (I say this as an ER doc), and etomidate and ketamine have larger safety profiles, so that adds another layer of safety for our patients.

Regardless, etomidate is not the boogie man.

 

[AdmiralChz]

Geesh sorry I walked back into this forum... too many of the discussions here in this sub forum are “EM vs everyone else” - can’t we just try to learn from each other rather than doc-on-doc attacks (“clings to propofol”)? Don’t even get me started on the ridiculous intubation d*ck waving.

I use etomidate nearly everyday in my CT Anesthesia fellowship, I see sickies literally every case. Works great for me, haven’t seen many develop acute adrenal insufficiency. But it’s important to be flexible, the other day we ran out of it and had to use alternative agents.

Some anesthesiologists hate etomidate. The post-op nausea/vomiting is the real deal and inhibits rapid discharge for outpatient procedures. The myoclonus can actually acutely increase BP and even worsen other injuries if severe enough in trauma.

My point originally was it’s typically the easiest medication to reach for in an acute emergency outside of the ER and OR. If attacking me or my colleagues makes you feel better, then go ahead I guess...

 

[RoyBasch]

I'm finding the anesthesia--particularly the cardiac anesthesia perspective pretty interesting.

 

[Angry Birds]

I respect our anesthesia colleagues and their valuable input. What I will say however is that there is a logic to reducing variables as much as possible while working in the ER.

The other day I had a young patient who came in full cardiac arrest. I code him and have ROSC... I’m intubating him while at the same time medically managing him. I’m even history taking at the same time as all of this. I have a wide complex tachycardia on the monitor and seizure report so now I guess that this is a TCA overdose and treat accordingly. These are complex patients and my mind is whirring all this time. Last thing I want to think about is what medication to call out for RSI, especially when I’m barking out other orders and drips to various nurses, some of whom I’ve never worked with before.

In such a chaotic environment, yeah I’m gonna call out Etomidate 30 mg and do what I’ve done for years. Adrenal suppression? This guy is on death’s doorbed.

 

[gutonc]

Geesh sorry I walked back into this forum... too many of the discussions here in this sub forum are “EM vs everyone else” - can’t we just try to learn from each other rather than doc-on-doc attacks (“clings to propofol”)? Don’t even get me started on the ridiculous intubation d*ck waving.

Well, to be fair, although the OP is in EM, much of the EM vs everyone else attitude in this thread has come in response to anesthesiologists coming here (the EM forum) to tell them how badly they're f-ing up. This is the kind of behavior that is actually forbidden in the ToS...

• Positive interactions between medical communities. The Student Doctor Network encourages members to engage in the wide variety of medical fields represented on the Forums. Open dialogue between medical professions promotes better understanding and working relationships. Please note, members that engage in attacking a specific field of medicine within that field’s forum may receive a warning or be banned from that forum. Forum members should encourage positive discussion between the professions.

The discussion has mostly turned itself around, but for awhile there it was bordering on thread closure/warning status.

So just keep it professional, and all will be fine.

 

[deleted547339]

Geesh sorry I walked back into this forum... too many of the discussions here in this sub forum are “EM vs everyone else” - can’t we just try to learn from each other rather than doc-on-doc attacks (“clings to propofol”)? Don’t even get me started on the ridiculous intubation d*ck waving.

I use etomidate nearly everyday in my CT Anesthesia fellowship, I see sickies literally every case. Works great for me, haven’t seen many develop acute adrenal insufficiency. But it’s important to be flexible, the other day we ran out of it and had to use alternative agents.

Some anesthesiologists hate etomidate. The post-op nausea/vomiting is the real deal and inhibits rapid discharge for outpatient procedures. The myoclonus can actually acutely increase BP and even worsen other injuries if severe enough in trauma.

My point originally was it’s typically the easiest medication to reach for in an acute emergency outside of the ER and OR. If attacking me or my colleagues makes you feel better, then go ahead I guess...

Did you not read the post I wrote immediately prior to yours? That was (mostly) a joke.

 

[AdmiralChz]

That was (mostly) a joke.

Was referring to the half-hearted roll back of the comment (as here...). I am sure you know inflexible ED physicians as well.

Anyway, tons of different ways to induce and there’s no one way that suits all. Be mindful of other options and their uses.

 

[Psai]

Well, to be fair, although the OP is in EM, much of the EM vs everyone else attitude in this thread has come in response to anesthesiologists coming here (the EM forum) to tell them how badly they're f-ing up. This is the kind of behavior that is actually forbidden in the ToS...

• Positive interactions between medical communities. The Student Doctor Network encourages members to engage in the wide variety of medical fields represented on the Forums. Open dialogue between medical professions promotes better understanding and working relationships. Please note, members that engage in attacking a specific field of medicine within that field’s forum may receive a warning or be banned from that forum. Forum members should encourage positive discussion between the professions.

The discussion has mostly turned itself around, but for awhile there it was bordering on thread closure/warning status.

So just keep it professional, and all will be fine.

What are you talking about?

 

[WildcatS11]

What are you talking about?

Other (previous) threads.

 

[deleted109597]

Let's not hash out old threads, and lets not fight this tired battle here.

 

[Apollyon]

Let's not hash out old threads, and lets not fight this tired battle here.

Is there going to be a mod fight??

 

[noise115]

Anesthesiologist here- I agree with most of what has been said. Etomidate is a fine drug for any intubation, provides the most hemodynamic stability when using a single induction medication (as opposed to midaz/fent/gas, etc). I would NOT use it for sedation (unprotected airway + incr risk of nausea/vom = no bueno).

I would say the main reason we do NOT use a lot etomidate is not adrenal suppression, myoclonus, nor our 'blind' preference for propofol. I don't routinely give etomidate because 90% of the patients I induce will wake up and be extubated the same day - sometimes the same hour I give my induction medications. Etomidate can and does increase PONV (postop nausea and vomiting) - so I would rather have a more elegant anesthetic by using propofol (a potent treatment for nausea in the short term, in addition to its other uses) and limit the amount of nauseating medications I give. Nothing worse than an admission for PONV after an outpatient procedure.

If I was intubating a hemodynamically unstable patient in the ED or ICU, where I can't slowly titrate medicaitons myself (I typically give prop + heavy opioid/BDZ + appropriate vasopressor/inotrope), then I would absolutely give Etomidate every time to keep it simple. Ketamine is a potent vasodilator and minor cardiac depressant and, similar to ephedrine, only releases endogenous NE/Epi/Dopamine when given which causes tachycardia and relative hypertension. If the patient has little or no more usable cathacholamines left due to over excitation of the SNS, then Ketamine becomes similar to propofol in hemodynamics.

It's all patient/situation specific. Every medication I give has a purpose in the OR, which I understand is sometimes a luxury.

 

[Groove]

Interesting thread. The only thing I love more than an optimal induction agent is an induction agent that is AVAILABLE which means I get to use etomidate 90% of the time for emergent intubations.

On a side note, are any of you sedating in the ED with dexmedetomidine? Honestly, I never heard of this stuff until the past few years. I don't recall ever seeing it used in residency but my current intensivisists frackin' (finishing last season of battlestar galactica atm) love the stuff. It doesn't matter what I start them on in the ED, they inevitably will switch them as soon as they get to the ICU.

 

[noise115]

Interesting thread. The only thing I love more than an optimal induction agent is an induction agent that is AVAILABLE which means I get to use etomidate 90% of the time for emergent intubations.

On a side note, are any of you sedating in the ED with dexmedetomidine? Honestly, I never heard of this stuff until the past few years. I don't recall ever seeing it used in residency but my current intensivisists frackin' (finishing last season of battlestar galactica atm) love the stuff. It doesn't matter what I start them on in the ED, they inevitably will switch them as soon as they get to the ICU.

It is an alpha-2 agonist similar to, but much more centrally acting than, clonidine. We use it in the OR for moderate sedation cases, anxiolysis for awake intubations (keeps spontaneous respirations), adjunctive analgesic, emergence agitation for children. I'm not positive how useful it would be in the more acute setting, but it is an interesting idea. Useful for ICU sedation as it provides some analgesia, allows for spontaneous respiration at most doses, and doesn't cause as much hypotension compared to propofol. Drawbacks are that it cannot make someone truly unconscious, its expensive most places, can cause significant bradycardia

 

[TheTruckGuy]

I'm still a resident, but I was taught to reach for etomidate and sux as my go to because of hemodynamics and rapid onset UNLESS I had a reason to go with something else. Someone looks like a dialysis patient/liver failure, maybe has hepatorenal going on, go with high dose Roc, for example.

I know ketamine is becoming more popular, and i've used it in the OR when on my anesthesia rotation. It definitely will cause a catecholamine release and increase in secretions. I had a normal, young, healthy patient go from about 110/70 to 220/something, and at the end of the case is mouth was full of secretions more than any other patient I saw on that rotation.
I've had attendings tell me they use etomidate for shoulder reductions at normal intubating doses (0.3mg/kg), which kinda scares me. But they say you just bag them a little if they lose complete respiratory drive. Still scares me.
But one thing I definitely like doing, and I think EM is great for it, is just knowing all your tools, how they work, and what you want to accomplish in different scenarios. Every now and again you may pick the less than ideal tool for the job, but if you know what you're doing it should be close enough to work.

 

[Apollyon]

frackin' (finishing last season of battlestar galactica atm)

Fracking as yet is not obscured by the censor, so, we're good.

 

[OB1🤙]

"It's not the wand, it's the wizard."

 

[deleted547339]

Interesting thread. The only thing I love more than an optimal induction agent is an induction agent that is AVAILABLE which means I get to use etomidate 90% of the time for emergent intubations.

On a side note, are any of you sedating in the ED with dexmedetomidine? Honestly, I never heard of this stuff until the past few years. I don't recall ever seeing it used in residency but my current intensivisists frackin' (finishing last season of battlestar galactica atm) love the stuff. It doesn't matter what I start them on in the ED, they inevitably will switch them as soon as they get to the ICU.

It’s good. Not great. But good. I don’t see a role for it in the ER.

 

[Siggy]

Drawbacks are that it cannot make someone truly unconscious, its expensive most places, can cause significant bradycardia

Why is the pulse in the 40s?
::checks sedation::
Um, I guess we need to D/C the precedex.

Also, technically speaking, it's only approved for 24 hours over concerns of patients developing tolerance.

 

[The Physician Philosopher]

Why is the pulse in the 40s?
::checks sedation::
Um, I guess we need to D/C the precedex.

Also, technically speaking, it's only approved for 24 hours over concerns of patients developing tolerance.

And if you use it for sedation as an infusion you can enjoy the accompanying hypotension for the next three to four hours, too. Pretty long context senstive half life.

Not the right drug for bolusing for deeper levels of sedation (i.e. induction). Good drug for sedation on patients that won't tolerate loss of respiratory drive seen with propofol, such as the pulmonary HTN patient. [There is evidence in anesthesia literature that dexmedatomidine has some respiratory depression.... But I think it was done on healthy volunteers where co2 was bled into the circuit... Don't buy it clinically]

Sent from my XT1710-02 using Tapatalk

 

[TheTruckGuy]

Why is the pulse in the 40s?
::checks sedation::
Um, I guess we need to D/C the precedex.

Also, technically speaking, it's only approved for 24 hours over concerns of patients developing tolerance.

Interesting. When I was on ICU I saw precedex running for days, often times combined with another agent, so not sure if that makes a difference.