Etomidate-- I think this needs its own thread

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Intubate

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This has come up in two threads recently. I haven't looked at all these papers yet(the section below is clipped from Blade MD). All the ones I looked at were in septic patients, but its concerning. To be fair, a "routine" patient and a septic patient are not the same, but its got to make you think.


Blade says:
Here are many peer reviewed articles on Etomidate and Critically ill patients.

Critical Care 2006;10 (4) R105
Critical Care 2007 April 35 (4) 1012-8
Critical Care 2007 May 24; 11 (3); R61

Another good study:

Chest 2005 March; 127 (3) 707-09

It seems if you use Etomidate (even a single low dose) MANY authors are recommending coverage with steroids.

Chest 2006; 10 (4): R105

This study recommends a moratorium on etomidate use period.
The two CHEST journal articles state that etomidate without steroid supplementation will cause 1in 5 patients that got the drug to DIE as a result. Pretty strong wording and a 20% mortality due to etomidate use!

The bottom line is pretty clear: Use etomidate at your own peril and if you use it at all YOU MUST GIVE STEROIDS for several days or more.



What do you guys think? Do you (like me) use etomidate on a regular basis? Are we killing people?
 
I had used Etomidate on my "sick" patients. They may arrive in the holding area from home but after the case many end up in the ICU for days.

Other patients come from the E.R. as trauma patients. Some end up on the floor and a few in the ICU.

From what I gather Etomidate use on patients sheduled to have routine surgery not requiring an ICU stay may be well tolerated and not lead to increased mortality. This category of patient could potentially receive etomidate without steroid supplementation.

Unfortunately, most of my patients needing etomidate fall into the definite or likely post-op ICU category and Not the short over-night stay.

Blade
 
I haven't used etomidate in 2 yrs now. I had an otherwise healthy guy with a compartment syndrome and low BP about 2 yrs ago that I gave etomidate to. It was his only dose and he had a severe case of adrenal supression. I have never used it since.

I just cut my propofol dose way down. Sometimes as low as 5 cc.
 
I have not looked at these article closely - but I have a question about them. If someone has looked closely, please reply.

Who was doing the airway securing in most of these patients? The reason I ask is because as anesthesiologists, we do things differently than an ICU or ER doc intubating. Most of the latter know a unit dosing - i.e. - a whole stick based on weight - whereas an anesthesiologist will base the dosing completely different. Another point is that we as autonomic system masters, if we see a post intubation slumb, we will fix it quickly, whereas the ICU or ER team is likely to "write an order, stand in the corner" if you know what i mean.

I think these questions are very important when looking at these studies, because a slug of etomidate and severe untreated hypotension may make a huge difference from 2 ccs of induction drug (just a dab will do....) and quick treatment of hemodynamics.

The other problem might be selection bias. The patients that are more unstable are more likely to get etomidate in the first place.

I know I originally brought up the issue in Blade's case, and I have thought a lot about it since Blade put up his follow up posts and then with the articles. I think it is a VERY interesting topic. I suppose the problem is that sometimes there might NOT be a great alternative. I have suggested a bunch of versed which can be very cardiac stable, but that isn't great in a 1 to 2 hr case if you want to extubate. Same with scopolamine - plus I have heard it doesn't really guarentee amnesia. I was reminded this week that propofol is only FDA approved for 40mg every 10 secs (no faster) or 20mg per 10 secs if you are over 65 - perhaps if I actually followed the FDA on propofol, I might be able to manage. Ketamine is a direct cardiac depresent - so sometimes it seems you are only left with etomidate.
 
I have not looked at these article closely - but I have a question about them. If someone has looked closely, please reply.

Who was doing the airway securing in most of these patients? The reason I ask is because as anesthesiologists, we do things differently than an ICU or ER doc intubating. Most of the latter know a unit dosing - i.e. - a whole stick based on weight - whereas an anesthesiologist will base the dosing completely different. Another point is that we as autonomic system masters, if we see a post intubation slumb, we will fix it quickly, whereas the ICU or ER team is likely to "write an order, stand in the corner" if you know what i mean.

I think these questions are very important when looking at these studies, because a slug of etomidate and severe untreated hypotension may make a huge difference from 2 ccs of induction drug (just a dab will do....) and quick treatment of hemodynamics.

The other problem might be selection bias. The patients that are more unstable are more likely to get etomidate in the first place.

I know I originally brought up the issue in Blade's case, and I have thought a lot about it since Blade put up his follow up posts and then with the articles. I think it is a VERY interesting topic. I suppose the problem is that sometimes there might NOT be a great alternative. I have suggested a bunch of versed which can be very cardiac stable, but that isn't great in a 1 to 2 hr case if you want to extubate. Same with scopolamine - plus I have heard it doesn't really guarentee amnesia. I was reminded this week that propofol is only FDA approved for 40mg every 10 secs (no faster) or 20mg per 10 secs if you are over 65 - perhaps if I actually followed the FDA on propofol, I might be able to manage. Ketamine is a direct cardiac depresent - so sometimes it seems you are only left with etomidate.

Okay, if and when you decide to use Etomidate then COVER the patient with steroids for 48-72 hours. If the patient ends up in the ICU steroid coverage is not a bad idea anyway. But, this also means INSULIN coverage (tight glucose control) may be needed as well.

Low dose propofol (50 mg) plus low dose ketamine (30 mg) should provide an alternative as an induction agent for many patients.

Blade
 
I have not looked at these article closely - but I have a question about them. If someone has looked closely, please reply.

Who was doing the airway securing in most of these patients? The reason I ask is because as anesthesiologists, we do things differently than an ICU or ER doc intubating. Most of the latter know a unit dosing - i.e. - a whole stick based on weight - whereas an anesthesiologist will base the dosing completely different. Another point is that we as autonomic system masters, if we see a post intubation slumb, we will fix it quickly, whereas the ICU or ER team is likely to "write an order, stand in the corner" if you know what i mean.

I think these questions are very important when looking at these studies, because a slug of etomidate and severe untreated hypotension may make a huge difference from 2 ccs of induction drug (just a dab will do....) and quick treatment of hemodynamics.

The other problem might be selection bias. The patients that are more unstable are more likely to get etomidate in the first place.

I know I originally brought up the issue in Blade's case, and I have thought a lot about it since Blade put up his follow up posts and then with the articles. I think it is a VERY interesting topic. I suppose the problem is that sometimes there might NOT be a great alternative. I have suggested a bunch of versed which can be very cardiac stable, but that isn't great in a 1 to 2 hr case if you want to extubate. Same with scopolamine - plus I have heard it doesn't really guarentee amnesia. I was reminded this week that propofol is only FDA approved for 40mg every 10 secs (no faster) or 20mg per 10 secs if you are over 65 - perhaps if I actually followed the FDA on propofol, I might be able to manage. Ketamine is a direct cardiac depresent - so sometimes it seems you are only left with etomidate.

You must be kidding about the propofol FDA timing. Try getting JPP "down" with that dosing scheme. It will be a long induction.:laugh:

Blade
 
Etomidate will remain one of the drugs I use once a while until they stop making it.
I have learned that studies are most of the times biased and done for motives other than science, and I can give you endless examples of studies that showed opposing results and caused the practice of medicine to swing back and forth, just think about the drug eluting stents and their controversy.
 
Etomidate will remain one of the drugs I use once a while until they stop making it.
I have learned that studies are most of the times biased and done for motives other than science, and I can give you endless examples of studies that showed opposing results and caused the practice of medicine to swing back and forth, just think about the drug eluting stents and their controversy.

Let me say this upfront: I like etomidate. It WAS my favorite induction agent for the critically ill or trauma patient. Not anymore. I looked for those studies defending the routine use of etomidate. What I found was "opinion' that etomidate's good outweighed its bad. There was no recent clinical evidence that etomidate was "safe" in septic pateints. There were studies (not biased) showing increased MORTALITY in trauma patients sent to the ICU (no steroid supplementation).

Again, I used to like etomidate a lot. Not so much anymore.

Blade
 
You must be kidding about the propofol FDA timing. Try getting JPP "down" with that dosing scheme. It will be a long induction.:laugh:

Blade


I only mentioned it because it suprised me. I also learned that volital agents are not FDA approved for pediatrics, Fentanyl is not approved for under age 2, and some other stuff i had no idea about.

It only reminded me that the FDA means little - which suprises me so much that when you ask people about why they don't use droperidol, they spout out something like "well the FDA bla bla bla.....", yet they violate the FDA rules every day - multiple times.
 
I only mentioned it because it suprised me. I also learned that volital agents are not FDA approved for pediatrics, Fentanyl is not approved for under age 2, and some other stuff i had no idea about.

It only reminded me that the FDA means little - which suprises me so much that when you ask people about why they don't use droperidol, they spout out something like "well the FDA bla bla bla.....", yet they violate the FDA rules every day - multiple times.

To clarify, the FDA will only approve a drug for the dose, population, route, etc which has been submitted by the drug company for approval & has studies to document its efficacy & safety within the parameters the company is seeking.

There are only a handful of drugs which are actually indicated in children & that population is broken down into ages 6-12, 2-6, less than 2 & neonatal. The reason they are not indicated is not because they can't be used - its only because there are no studies to support is use, dose, frequency, etc.. It is extremely expensive & requires far more elaborate IRB permission to conduct drug studies in infants & children, although the FDA is requiring the drug companies to expand their population age ranges so we don't rely on post-marketing surveillance alone for safety data. Just because there is no "official" indication doesn't mean the drug can't be used effectively & safely in any particular population.

Most drugs used in children & many, many drugs used in the population in general are used/prescribed "off label" which is perfectly acceptable & done all the time. Some drug companies have gotten into trouble advocating "off label" use, which they cannot do. However, there is absolutely nothing wrong in physicians using the drugs off label & in fact, that is often how we find how the drug is actually used in these populations - when physicians publish their case reports which then generates more study. These physicians are not "violating" any rules because a physician can prescribe any drug within the scope of his/her practice how he/she sees fit.

The FDA approved indication is a different thing than the "black box" warning which I think you were referring to with droperidol.

The "black box" is the strongest warning the FDA can apply to a drug without actually limiting its prescribing (like isotrentoin or thalomid). The "black box" is only there to focus a prescribers attention to a more frequent occurrance of a side effect which might have significant morbidity or mortality. The "black box" is often placed on a drug after these side effects appear in post-marketing surveillance. It is not to limit your use of the drug - only to bring your attention to a potential problem you might not have been aware of.

Now - why droperidol after all these years, you might ask. Well - droperidol used to be used in hospitals exclusively for decades. These pts were monitored & followed by physicians such as yourselves who were used to the arrhythmias &/or susceptible populations which might be inclined toward arrhythmia development.

But, in the last 10 years or so, we've had a huge increase in its outpt use in outpt surgery settings; oral surgeons, dermatologists, plastic surgeons & even FM folks who might be doing cosemetic work in their offices; & outpt pedi procedures. This has generated reports of more adverse reactions to the FDA. The actual percentage has not probably increased - its use has just increased and some might say by those folks who perhaps don't have the monitoring equipment &/or skills to deal with the potential side effects. Those of you old enough might remember Innovar which was a good drug, but was removed from the market because of deaths, many which occurred in dental offices. Psychiatrists don't worry about the black box on SSRIs, but its important for FM, Ob-gyn, peds, etc to be aware of them.

Unfortunately, some hospitals & P&T committees will take a "black box" warning & decide they don't want to carry the drug, even though the same population which had used it without issue for years & years is hindered by not keeping it on the formulary. That is short sighted - just my personal opinion.

I hope this clarifies what is meant by FDA approved indications & the significance of black box warnings.
 
The FDA approved indication is a different thing than the "black box" warning which I think you were referring to with droperidol.

Actually, no. Droperidol has no FDA indication for dosages below 2.5mg, so when we use it at 0.625mg, we are using it off label - hence the blackbox warning does not apply. (They even said so!)

Now - why droperidol after all these years, you might ask.

That is an excellent question, one that T.G Gan, PF White, C Apple, and other leading authors on PONV can't answer.

Here is a little graph I like to think about that makes me question the FDA.

# of peer reviewed case reports of cardiac events from droperidol at PONV dosing = NONE (with 30+ years of usage)

# of peer reviewed case reports of cardiac events from 5HT3 drugs at PONV dosing = many and still counting (with 10+ years of usage).
 
Okay, if and when you decide to use Etomidate then COVER the patient with steroids for 48-72 hours. If the patient ends up in the ICU steroid coverage is not a bad idea anyway. But, this also means INSULIN coverage (tight glucose control) may be needed as well.

Low dose propofol (50 mg) plus low dose ketamine (30 mg) should provide an alternative as an induction agent for many patients.

Blade


Execellent point. Would you use dexamethasone (30:1 anti-inflamatory:minercoricoid) or hydrocortisone which is 1:1?

Does hydrocortisone have anti-yak properties?
 
Can a single dose of dexamethasone lead to avascular necrosis? I've heard that it can, but I'm too lazy to look up the literature right now.
 
Can a single dose of dexamethasone lead to avascular necrosis? I've heard that it can, but I'm too lazy to look up the literature right now.

Yes. But, the incidence is very low. Remember this point when giving Decadron 4mg I.V. to EVERY patient getting a GA.

Blade
 
Execellent point. Would you use dexamethasone (30:1 anti-inflamatory:minercoricoid) or hydrocortisone which is 1:1?

Does hydrocortisone have anti-yak properties?
You use hydrocortisone because you are trying to compensate for mineralocoticoid activity not gluco corticoid, and anti inflammatory activity is irrelevant
 
Actually, no. Droperidol has no FDA indication for dosages below 2.5mg, so when we use it at 0.625mg, we are using it off label - hence the blackbox warning does not apply. (They even said so!)



That is an excellent question, one that T.G Gan, PF White, C Apple, and other leading authors on PONV can't answer.

Here is a little graph I like to think about that makes me question the FDA.

# of peer reviewed case reports of cardiac events from droperidol at PONV dosing = NONE (with 30+ years of usage)

# of peer reviewed case reports of cardiac events from 5HT3 drugs at PONV dosing = many and still counting (with 10+ years of usage).

Indeed your point is well taken, however, as your colleague S. Shafer from the Palo Alto VA in 2004 pointed out:

http://www.anesthesia-analgesia.org/cgi/content/full/98/2/551?ck=nck

The incidence of low dose droperidol & torsade will probably never be established due to the cost of drug trials & its incidence. Therefore, without definitive data, you look at case reports & the animal data & make the best judgement possible as an individual physician.

The FDA, however, must make the best decision for the safety of millions of people & knowing that providers, who don't have your skills, experience nor equipment, may use the drug without knowing the potential for risk.

The black box warning is for this purpose. It does not prevent you from using the drug. In fact, my hospital stocks it & keeps it available in pyxis - just not on those units without monitors (which are few). Altho the use of it has decrease 90%, it is still readily available.

I'm guessing its caution, as with etomidate, which has changed usage patterns - not FDA "rules" (there are none for providers). Unfortunately, this caution has made it difficult for younger physicians to gain experience with it - similar to etomidate.

However..this is way too off topic since this thread is about etomidate, not droperidol. I apologize. I agree with Plankton - there is so much "hidden" in drug studies its difficult to sort out agendas apart from information. We've lost some good drugs & still have some not so good drugs available because of this very reason.
 
I hate this stuff. A nice slow controlled induction with minimal propfol can get the job done without destroying your pressure.
 
Anyone ever split induction doses using etomidate (.1mg/kg) + propofol (1mg/kg)? One attending does this with cv cripples to decrease the hypotension you get with straight propofol.
 
Anyone ever split induction doses using etomidate (.1mg/kg) + propofol (1mg/kg)? One attending does this with cv cripples to decrease the hypotension you get with straight propofol.

Versed is also a very stable induction agent. I used this on heart pts regularly.
 
So, in the SICU where I'm working, they pretty much use Etomidate most of the time (all of the times I've been present) when needing to intubate a pt emergenty. And, this includes the anesthesiologists that come up for our difficult-to-intubate pts.

BUT, in searching, it seems that DOSING varies heavily depending on the provider.

The stated dose of 0.2-0.3mcg/kg doesn't always seem to apply from the anecdotes I've picked up on my searches. Highly operator dependent, it seems......

So, in an otherwise non-sedated patient whom either failed extubation or develops respiratory distress, what dose of Etomidate would you use to induce? Also, say you also could push some Versed with the Etomidate? (which this institution seems to almost always do during such instances)

Thanks for the input in advance.
 
So, in an otherwise non-sedated patient whom either failed extubation or develops respiratory distress, what dose of Etomidate would you use to induce? Also, say you also could push some Versed with the Etomidate? (which this institution seems to almost always do during such instances)

Thanks for the input in advance.

There isn't a dose I would use. I haven't pushed that crap in over 3 yrs.

And why in the world would they give versed b/4 giving etomidate? Are they afraid the etomidate might not work?:smack: F'in stupid.

At least you are here CF so that you can teach them.
 
I love versed as an induction agent. Rock solid hemodynamics. Often, you have to paralyze to get them to stop breathing though.

Do you give it with narcotics and worry about the negative hemodynamic effects when combined with narcotics?
 
There isn't a dose I would use. I haven't pushed that crap in over 3 yrs.

And why in the world would they give versed b/4 giving etomidate? Are they afraid the etomidate might not work?:smack: F'in stupid.

At least you are here CF so that you can teach them.

I honestly don't know about the versed with etomidate..... perhaps to minimize the dose of etomidate and thus an attempt to mitigate adrenal insufficiency???
 
never use the stuff (etomidate).

Just last night intubated someone in ICU with 2 mg of versed, 100mcg fentanyl and 50 mg of zemuron. The sicker they are the less drug u need.
 
Rarely if ever do I use it. If I do, I mix it 50/50 with propofol.

I would argue that in the ICU, where patients are often adrenally insufficient, etomidate may further impair the catecholamine producing adrenals.
 
I'm in internship and at our hospital everyone seems to use 2mg Versed and 20-30mg Etomidate. That is kinda what is de facto in addition to dealing with a shortage of other agents. We have very little supply of propofol. Got an email from the university hospital where I'll be for the CA years and formerly the only induction agent they had left was Etomidate, but they have just received a supply of Brevital...
 
I'm in internship and at our hospital everyone seems to use 2mg Versed and 20-30mg Etomidate. That is kinda what is de facto in addition to dealing with a shortage of other agents. We have very little supply of propofol. Got an email from the university hospital where I'll be for the CA years and formerly the only induction agent they had left was Etomidate, but they have just received a supply of Brevital...

Versed not needed and too much Etomidate.
 
What would you suggest for intubating the hypotensive, possibly septic patient, if Etomidate isn't that great of choice and you don't have propofol?
 
There isn't a dose I would use. I haven't pushed that crap in over 3 yrs.

And why in the world would they give versed b/4 giving etomidate? Are they afraid the etomidate might not work?:smack: F'in stupid.

During internship I was witness to maybe 20-30 crashing ICU patient induction/intubations, and first crack at the airway in maybe 5 of them. In nearly every case this is how it unfolded.

The attending (all Pulm/CC folks) asked for Versed (didn't say dose) and Etomidate (didn't say dose) to the bedside RN.

Minutes later, 2mg of Versed would show up, as would 20mg of Etomidate.

When ordered, the bedside RN would push the 2mg Versed, followed by a 10mL NS flush, into an otherwise capped IV.

Then, 30 seconds later, attending orders the 20mg Etomidate, again just flushed into an otherwise capped IV. Then, I **** you not, 30 seconds later, attending says, "Let's take a look" into the larynx of a spontaneously ventilating, mildly sedated patient, who was not surprisingly quite resistant to a good DL...or two...or three.

Attending then asks for vec. Minutes later, vec shows up, attending asks for either "4" or "6" [mg or mL? doesn't matter!], again bolused into a capped IV followed by 10ml NS flush, and eventually a very combative patient gets an ETT passed through their very edematous larynx.

Point of all this is -- I don't think these folks do think about why they give which meds, and when, and how, and in what order and with what timing. I mean, they collectively refer to any benzo/prop drip + any opioid drip as "the sedation" when it comes to ventilated patients. And even though a lot of Pulm/CC folks are very on board with adrenal suppression they nonetheless use etomidate with abandon since they are scared sh*tless of propofol-induced hypotension.
 
they nonetheless use etomidate with abandon since they are scared sh*tless of propofol-induced hypotension.

I guess you haven't been introduced to the trauma team at our institution yet...

One time one of our attendings pushed propofol and they started freaking out until he told them "etomidate comes in white now"
 
What would you suggest for intubating the hypotensive, possibly septic patient, if Etomidate isn't that great of choice and you don't have propofol?

We don't have etomidate, and most of these patients don't need propofol anyway.
Couple of mg of midaz, 100mcg fentanyl, and your choice of sux or roc.
 
I guess you haven't been introduced to the trauma team at our institution yet...

One time one of our attendings pushed propofol and they started freaking out until he told them "etomidate comes in white now"

:laugh::laugh::laugh:
Love it!
 
And even though a lot of Pulm/CC folks are very on board with adrenal suppression they nonetheless use etomidate with abandon since they are scared sh*tless of propofol-induced hypotension.

Have you ever witnessed a pulmonologist push a cc or three of phenylephrine? Me neither ... so I think their terror of propofol-induced hypotension is appropriate and well grounded. 😀

I quit arguing with the ER and ICU about etomidate inductions when I realized they're just not equipped to handle the side effects of propofol or choose a reasonable dose in the first place. Etomidate is safer in their hands, adrenal suppression or no. To them, giving a pressor means writing an order, waiting for the pharmacy to tube a bag, and then waiting for the nurse to put it on a pump. When they see 70/30 after induction, the only pushable pressor they've got is the epi in the crash cart.
 
Look, a favorite saying of mine is "Ive never not been able to intubate a patient because they werent sedated enough"

SO, if you have time to plan, a little fentanyl (remifentanyl?) + versed coupled with paralytic can augment low dose propofol.

Now, in the OR, we still use a fair amount of etomidate, and Ill admit to using it on patients where Im worried about the narrow range between too much sedation (hypotension) and not enough (tachycardia/hypertension)

all roads lead to rome, however
 
What would you suggest for intubating the hypotensive, possibly septic patient, if Etomidate isn't that great of choice and you don't have propofol?

Etomidate is probably fine, by the way, this is from CHEST 7/22/10

Outcomes of Etomidate in Severe Sepsis and Septic Shock


Background: The use of single-dose etomidate to facilitate intubation in critically ill patients has recently been debated given its suppression of steroidogenesis with possible resultant adverse outcomes. Our objective was to assess the effects of single-dose etomidate used during rapid sequence intubation on various measures of outcome such as mortality, vasopressor use, corticosteroid use, ICU-length of stay and number of ventilator-days.

Methods: A retrospective 18-month cohort study was performed in a multidisciplinary ICU of an academic tertiary care institution. Consecutive patients with severe sepsis or septic shock who were intubated and mechanically ventilated were identified and grouped as having received single-dose etomidate during intubation or not. Hospital mortality, ICU length of stay, number of ventilator-days, corticosteroid use, vasopressor use, as well as demographic and clinical variables were recorded.

Results: A total of 224 patients were identified; 113 had received etomidate. The mean APACHE II scores in the etomidate and non-etomidate groups were 21.3 +8.1 and 21.9 +8.3 respectively (p=0.62). The relative risks for mortality and vasopressor use were 0.92 (C.I. 0.74-1.14, p=0.51) and 1.16 (C.I. 0.9-1.51, p= 0.31) respectively, in the etomidate group. There were no significant differences in ICU-LOS (Mean 14 versus 12 days, p=0.31) or number of ventilator-days (Mean 11 versus 8 days, p=0.13) between the etomidate and non-etomidate groups, respectively. The relative risk for corticosteroid use in the etomidate group was 1.34 (C.I. 1.11-1.61, p=0.003). Multivariate analysis using logistic regression demonstrated no significant association of etomidate with mortality (OR 0.9, C.I. 0.45-1.83, p=0.78).

Conclusion: Single-dose etomidate used during rapid-sequence intubation in critically ill patients with severe sepsis and septic shock was not associated with increased mortality, vasopressor use, ICU-LOS or number of ventilator-days. Patients intubated with etomidate had an increased incidence of subsequent corticosteroid use, with no difference in outcomes.
 
A question from a lurker:

What do you all think of ketamine before sux or roc in the old, hypotensive, crashing spetic patient?

HH
 
Probably not a good idea. Ketamine carries that risk of direct myocardial depression so in someone with maxed out catecholamine secretion who likely doesnt have much sympathetic reserve to rely on, I could see them doing poorly. Some versed should work nicely.
 
We use everyday in the heart room and don't give follow up steroids for the next 48-72 hrs. I'm w/idio on this one, I don't think a single dose will make a huge difference
 
I haven't used etomidate in over 5 years. I just haven't found much of a place for it. I find propofol in the appropriate dose to be pretty hemodynamically stable. Sometimes the old patients might just get about 30-40 mg. With versed for amnesia. And if they are actually unstable and hupotensive then I will use just some versed and muscle relaxant. I have sort of forgotten about this drug! But I don't do hearts anymore so maybe some of the heart guys use it.
 
Versed not needed and too much Etomidate.

So how much do you give? The recommended dosing range is 0.2-0.6mg/kg. The dose I give depends on the overall clinical picture (other recent drugs administered, hemodynamic state, current mental state, etc), but I've been told "never give more than 20mg" which just seems odd, since on a typical guy 0.3mg/kg is 21mg.

So how much do you guys routinely give and why?
 
So how much do you give? The recommended dosing range is 0.2-0.6mg/kg. The dose I give depends on the overall clinical picture (other recent drugs administered, hemodynamic state, current mental state, etc), but I've been told "never give more than 20mg" which just seems odd, since on a typical guy 0.3mg/kg is 21mg.

So how much do you guys routinely give and why?

If I ever use Etomidate (which is rare these days) I would give 0.2 mg/kg with a muscle relaxant.
 
I don't think these folks do think about why they give which meds, and when, and how, and in what order and with what timing. I mean, they collectively refer to any benzo/prop drip + any opioid drip as "the sedation" when it comes to ventilated patients. And even though a lot of Pulm/CC folks are very on board with adrenal suppression they nonetheless use etomidate with abandon since they are scared sh*tless of propofol-induced hypotension.

Every hospital i have been in has a policy that only gas could bolus propofol.

Have you ever witnessed a pulmonologist push a cc or three of phenylephrine? Me neither ... so I think their terror of propofol-induced hypotension is appropriate and well grounded. 😀

I quit arguing with the ER and ICU about etomidate inductions when I realized they're just not equipped to handle the side effects of propofol or choose a reasonable dose in the first place. Etomidate is safer in their hands, adrenal suppression or no. To them, giving a pressor means writing an order, waiting for the pharmacy to tube a bag, and then waiting for the nurse to put it on a pump. When they see 70/30 after induction, the only pushable pressor they've got is the epi in the crash cart.

I know one pulm-cc doc who will carry neo syringes with him, but only one and he did a ton of SICU time, but again, hospital policies make it difficult as they don't want us mixing drips/meeds on the floor. Just sunday night i got chewed on for having a nurse put an amp of bicarb in a bag of D5w by pharmacy 🙄

But it sounds to me at you guys are making much too big a deal about etomitdates adrenal suppression, the outcome data on etomidate especially in sepsis isn't that great, especially when we're moving away from using steroids in sepsis yet again.
 
Im not saying its a great drug, and you do get significant adrenal suppression with it, so I can understand why the postop hearts get hypotensive and refractory to catecholamines when they take them and diurese the crap out of them coupled with adrenal suppression, no matter how transient.

ironically enough, i find that the hearts are probably the one patient group that SHOULDNT get etomidate, at least where i trained
 
I had used Etomidate on my "sick" patients. They may arrive in the holding area from home but after the case many end up in the ICU for days.

Other patients come from the E.R. as trauma patients. Some end up on the floor and a few in the ICU.

From what I gather Etomidate use on patients sheduled to have routine surgery not requiring an ICU stay may be well tolerated and not lead to increased mortality. This category of patient could potentially receive etomidate without steroid supplementation.

Unfortunately, most of my patients needing etomidate fall into the definite or likely post-op ICU category and Not the short over-night stay.

Blade

So, other than the adrenal suppression, are there other reasons to steer clear of this drug??

I'm just sayin, cause on SICU rounds the other day, both the intensivist (CCM and CT fellowed anesthesiologist) and the PharmD in the ICU both dismissed "one or two" small doses of etomidate as concern for adrenal insufficiency......

I'm just trying to make sense of this in lieu of some very strong negative opinions on this forum.

cf
 
Miller pretty clearly states that a single dose of etomidate impairs steroidogenesis for 48-72 hours. It certainly wont affect everybody, but if you have big fluid shifts to contend with and you factor in that the patients you are usually giving etomidate to in the operating room are perceived as sicker, in one way or another, then theres a big reason why it gets hated on.
 
So, other than the adrenal suppression, are there other reasons to steer clear of this drug??

Great board question derived from this. I think the factor most likely to cause people to rate anesthesia with etomidate as unsatisfactory is the high rate of PONV, but also pain on injection and myoclonus and EEG changes (but no ACTUAL seizures)

Etomidate is a safe drug, has minimal myocardial depression at clinical doses and while it has its own side effects, it doesnt carry the risk of significant myocardial depression (ketamine, propofol) or of being a controlled substance (versed, fentanyl)
 
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