How would you induce?

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loveumms

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So, I had a very interesting case today. Basically, EGD for achalasia.

Pt is 60s, HTN, CAD s/p stents, atrial flutter, chronic steroid use for lupus, anemia, thrombocytopenia. Here is where it gets dicey. Severe aortic stenosis on echo (valve area of 0.9) with mitral regurgitation. However, on cardiac cath, pt is found to only have mild aortic stenosis with a gradient of 5mmHg. She gets to the holding area and is tachy. Floor has given her two doses of metoprolol.

So ... how would you induce? How do you decide if she truly has aortic stenosis?
 
patient needs to have better rate control of her flutter before arriving to holding. back to floor for medicine to increase beta blockers or CCB, etc.

AS: cath is GOLD standard. but, assume she has severe AS - use etomidate and have phenylephrine ready. keep HR low. another reason to have better rate control prior to this ELECTIVE procedure.

RSI with Etomidate/Succ. Esmolol and lidocaine IV upfront.
 
Etomidate is really a crappy drug and I would avoid it if possible.
Here is what I would do:
Spray the throat with Benzocaine or Lidocaine or whatever you like then give Little increments of Propofol with nothing else and tell the patient to swallow until the scope is in the esophagus and everything is suctioned out, then give a little bit more propofol and let the GI guy do his thing.
Keep it simple.
 
Etomidate is really a crappy drug and I would avoid it if possible.
Here is what I would do:
Spray the throat with Benzocaine or Lidocaine or whatever you like then give Little increments of Propofol with nothing else and tell the patient to swallow until the scope is in the esophagus and everything is suctioned out, then give a little bit more propofol and let the GI guy do his thing.
Keep it simple.

I'm with Plank on this one -- have done several similar patients in the past just like this. However, I would want to control the heart rate first. EGD for achalasia doesn't sound like an emergency.
 
patient needs to have better rate control of her flutter before arriving to holding. back to floor for medicine to increase beta blockers or CCB, etc.

AS: cath is GOLD standard. but, assume she has severe AS - use etomidate and have phenylephrine ready. keep HR low. another reason to have better rate control prior to this ELECTIVE procedure.

RSI with Etomidate/Succ. Esmolol and lidocaine IV upfront.

Cath is not the gold standard. I don't believe that and neither do the ACC/AHA guidelines. It will always underestimate the gradient and the number they report is completely nonphysiologic. Echo is the gold standard in my book. It will give you an instantaneous gradient, the AV area, MR severity, filling pressures, CO, etc. If the echo says the AVA is 0.9, you know that's the biggest it's going to be. It could be smaller if they didn't catch the jet right on. I'd also be concerned if she had any symptoms which would make her AS critical and not severe and indicate a need for AVR, but that's another story.
 
Tachy? How tachy is the pt. Jeff05, you surely can send the pt back to medicine to get better rate control or you can do it yourself. If you do it yourself you will be home sooner an more importantly the pt will get his needed procedure. I fyou send him to medicine they won't get control of it for hours. Now you are doing it later in the day when other things have come up or your partner is having to deal with it the next day. Either way is no bueno.

I don't use etomidate. I believe it is a poor drug. I would do as Plank mentioned with propofol and possibly some ketamine mixed in as well.
 
Etomidate is really a crappy drug and I would avoid it if possible.
Here is what I would do:
Spray the throat with Benzocaine or Lidocaine or whatever you like then give Little increments of Propofol with nothing else and tell the patient to swallow until the scope is in the esophagus and everything is suctioned out, then give a little bit more propofol and let the GI guy do his thing.
Keep it simple.

I don't use etomidate. I believe it is a poor drug. I would do as Plank mentioned with propofol and possibly some ketamine mixed in as well.

👍

And, while a valve area of 0.9 is "critical" by definition, the thickness of the LV myocardium and the patient's symptomology is more important. If you have someone who gets short of breath walking across the room, then you're in deep doo-doo. If you have someone with a thick left ventricle, then you are in deep doo-doo. The fact that she tolerates flutter with RVR and hasn't died yet is, believe it or not, actually a pretty good predictor that she'll tolerate the procedure... given the techniques above. No need for an endotracheal tube in this case.

-copro
 
Pent, sux , tube
 
would you guys elaborate why you don't like etomidate? thanks in advance...

Nasty drug with bad side effects like nausea, vomiting and adrenal depression. Many believe AD only happens with repeat doses but I have seen it with one dose only. You can achieve the same outcome with propofol the vast majority of the time if you dose it carefully enough and give it time to work. Even if it is a RSI. I wouldn't go so far as to say etomidate should never be used but I haven't used it in over 3 yrs.
 
Given her chronic steroid use is the adrenal suppression from etomidate still a significant factor to consider?
 
my response is not "real world." it's how the aba wants this done.

high risk patient who is not optimized for an elective procedure - send back for optimization.

full stomach situation - RSI. period.

you have someone with poor rate control with CAD and severe AS. increased myocardial demand and a CO that is preload dependent (needs diastolic filing time). heart rate control is ESSENTIAL in this patient.

they gave her beta blockers already. that hasn't worked. sure, you can give more. are you willing to load her with CCB if beta blockade does not control rate? with dig? with amio? will your choices be best for OVERALL management of this patient? or is it just fudging it for the case?

no tube? ok. in someone else a pc02 of 60 (ph 7.25ish) and sats dropping to high 80s is ok. in her, it is not. (myocardial DO2 and excitability).

you give her propofol? her MAP will drop like a rock. SVR is already maximally constricted to maintain MAP in the face of fixed (low) CO. her diastolic pressure is now lower (decreased LV perfusion pressure). you can't give her enough analgesia to effectively blunt response to scope because that dose will make her apneic, so you will have to deal with more tachycardia. ditto if you give her ketamine.
pentathol may cause systemic vasodilation from histamine release - also undesirable in the setting of AS and CAD.

the situation now is that you have a patient with CAD and AS who is even MORE tachycardic, hypotensive, acidotic, and hypoxic (her myocardial oxygen balance is...unfavorable): for an elective procedure. you just failed the oral boards.


my oral board answer:
you give her something to slow her down best you can.
send her back to medicine. they optimize rate control.
she comes down in 2 days with good rate control.
you induce with a drug that will minimize hypotension. maybe you go absolutely nuts and pop in an a line prior to induction (all of 2 minutes) - which IS indicated. so RSI with etomidate/sux + IV lidocaine to blunt response to laryngoscopy.
keep BP up with phenylephrine as needed.
extubate when awake.
 
I forgot to mention the patient has sick sinus syndrome.

So, this is what we did. Patient came down, luckily the GI doc wasn't ready. I instructed the nurses to get her back up on the floor and give more metoprolol to get her HR down. Looking over the records, I noticed that on the floor she was 70s. She comes back down two hours later, is complaining of some pain. We give her some morphine to see if maybe decreasing her pain will decrease her HR. HR still 120s. Her BP is rock solid stable. I was thinking that we should maybe try something else like a CCB but, we talked it over and the patient was stable. We decide to just give lido jelly to numb up the pharynx then use a TOUCH of propofol, get the scope in and then keep BP up as needed.

In walks the GI doc. He notifies us that on barium swallow the patient was found to have a TON of debris in the esophagus. Well, there goes that plan. Now we have to do GA with ETT, RSI.

So, we do an awake a-line with just a touch of midaz and local infiltration. BP still rock stable. 2mg of etomidate at a time until patient loses eyelash reflex. Use a total of 6mg. Sux, RSI. intubation on first try (even though she could have been a difficult intubation with a receding chin). Tube is in, BP still stable (MAPs 90). Just a touch of sevo (MAC 0.4-0.5). Start procedure, BP drops slightly but little bits of phenylephrine keep it up. No reflex bradycardia with phenylephrine either.

Thank God we intubated this lady. You should have seen what they were sucking out of the esophagus. Chunks of food with lots of barium. I will always intubate a patient with achalasia after seeing this.

Then my attending changes to a CT anesthesiologist. He is very concerned about the HR (as was I at the start since we know she has CAD ... severe AS and oxygen consumption was crucial to maintaining her myocardium). We give 5 more of metoprolol, still no budge in HR. Sticks at 120s. He was considering giving some adenosine but, then the GI docs finish up and we extubate smoothly with minimal BP alteration. To PACU, A-line out patient stable.

Very cool case. Any further thoughts?
 
sounds like my plan worked.

I forgot to mention the patient has sick sinus syndrome.

So, this is what we did. Patient came down, luckily the GI doc wasn't ready. I instructed the nurses to get her back up on the floor and give more metoprolol to get her HR down. Looking over the records, I noticed that on the floor she was 70s. She comes back down two hours later, is complaining of some pain. We give her some morphine to see if maybe decreasing her pain will decrease her HR. HR still 120s. Her BP is rock solid stable. I was thinking that we should maybe try something else like a CCB but, we talked it over and the patient was stable. We decide to just give lido jelly to numb up the pharynx then use a TOUCH of propofol, get the scope in and then keep BP up as needed.

In walks the GI doc. He notifies us that on barium swallow the patient was found to have a TON of debris in the esophagus. Well, there goes that plan. Now we have to do GA with ETT, RSI.

So, we do an awake a-line with just a touch of midaz and local infiltration. BP still rock stable. 2mg of etomidate at a time until patient loses eyelash reflex. Use a total of 6mg. Sux, RSI. intubation on first try (even though she could have been a difficult intubation with a receding chin). Tube is in, BP still stable (MAPs 90). Just a touch of sevo (MAC 0.4-0.5). Start procedure, BP drops slightly but little bits of phenylephrine keep it up. No reflex bradycardia with phenylephrine either.

Thank God we intubated this lady. You should have seen what they were sucking out of the esophagus. Chunks of food with lots of barium. I will always intubate a patient with achalasia after seeing this.

Then my attending changes to a CT anesthesiologist. He is very concerned about the HR (as was I at the start since we know she has CAD ... severe AS and oxygen consumption was crucial to maintaining her myocardium). We give 5 more of metoprolol, still no budge in HR. Sticks at 120s. He was considering giving some adenosine but, then the GI docs finish up and we extubate smoothly with minimal BP alteration. To PACU, A-line out patient stable.

Very cool case. Any further thoughts?
 
i know what you're saying. but, i think that the best plan is one that requires the appropriate amount of intervention.


One thing I have learned over the years: the best anesthetic plan is the one that requires the least amount of intervention.
 
So a rapid sequence induction is done by titrating etomidate gradually to loss of lid reflexes then giving Sux?
Who is teaching you this stuff?

I have to say that this sounds kind of strange to me. Titrating in such small amounts in a slow manner sort of obviates the whole definition of a "rapid sequence induction". 6 mg of etomidate doesn't sound like it would blunt the response to laryngoscopy much, although you did say that you used some lido first.
 
i know what you're saying. but, i think that the best plan is one that requires the appropriate amount of intervention.

😀
The good news is that you will pass your boards most likely (unless I was your oral examiner), but then you will have to relearn anesthesia if you go to private practice.
 
😀
The good news is that you will pass your boards most likely (unless I was your oral examiner), but then you will have to relearn anesthesia if you go to private practice.

you're telling me that you would not have passed me if i laid out the above plan? and WOULD have passed me if i would have done what you suggest?
 
you're telling me that you would not have passed me if i laid out the above plan? and WOULD have passed me if i would have done what you suggest?
Yes,
Because I think that the oral exam should be about your ability to do things in the real world not about your ability to recite academic dogma.
By the way, you will soon find out that there are many young examiners on the oral board who share my view.
 
below is not a passing answer. i mean you would have to be a really junior examiner (like a ca1) to actually consider that adequate. it does not demonstrate knowledge of anesthetic considerations or co-existing dz.

maybe my answer wouldn't be what you would do, but it is definitely the RIGHT answer for the boards.


"Etomidate is really a crappy drug and I would avoid it if possible.
Here is what I would do:
Spray the throat with Benzocaine or Lidocaine or whatever you like then give Little increments of Propofol with nothing else and tell the patient to swallow until the scope is in the esophagus and everything is suctioned out, then give a little bit more propofol and let the GI guy do his thing."
 
below is not a passing answer. i mean you would have to be a really junior examiner (like a ca1) to actually consider that adequate. it does not demonstrate knowledge of anesthetic considerations or co-existing dz.

maybe my answer wouldn't be what you would do, but it is definitely the RIGHT answer for the boards.
"
Hey, I did say that you most likely would pass the boards with your answer because most of the examiners expect you to recite all that imaginary stuff they taught you in residency.
On the other hand there are plenty of people who might think that the best way to avoid a hemodynamic disaster in a patient with the above mentioned problems would be to avoid creating that disaster by administering an unnecessary anesthetic for a minor procedure that can be done under topical anesthesia with mild sedation.
That's just my humble opinion and you really don't have to even read it.
 
Hey, I did say that you most likely would pass the boards with your answer because most of the examiners expect you to recite all that imaginary stuff they taught you in residency.
On the other hand there are plenty of people who might think that the best way to avoid a hemodynamic disaster in a patient with the above mentioned problems would be to avoid creating that disaster by administering an unnecessary anesthetic for a minor procedure that can be done under topical anesthesia with mild sedation.
That's just my humble opinion and you really don't have to even read it.

YOU know that you are wrong with regards to the Oral Boards, right? You also know that there are many ways to skin a cat, right? If the approach makes clinical sense, like etomidate does, then you must pass. Oral boards is not about reading the examiners mind. It's about answering in a clinically relevant, well thought out plan, and being able to adjust. It doesn't matter how you do the case but that you can support your approach and that it is reasonably safe.
 
YOU know that you are wrong with regards to the Oral Boards, right? You also know that there are many ways to skin a cat, right? If the approach makes clinical sense, like etomidate does, then you must pass. Oral boards is not about reading the examiners mind. It's about answering in a clinically relevant, well thought out plan, and being able to adjust. It doesn't matter how you do the case but that you can support your approach and that it is reasonably safe.

Is this addressed to me?
I am wrong with regards to the oral boards in what aspect?
Where did I say that there is only one way to do anything? I am just presenting my way of doing this case and nothing further.
You don't think it is defensible on the boards to say that you chose to apply topical anesthesia and do mild sedation without abolishing the airway reflexes to do this case?
 
So a rapid sequence induction is done by titrating etomidate gradually to loss of lid reflexes then giving Sux?
Who is teaching you this stuff?


I was just going to say the same thing. Every time my attendings have used etomidate during RSI, the whole stick goes in without hesitation in two seconds.
 
Hey Plank- I realize disparaging academic anesthesiology is a favorite past time of yours but don't think every place is so dogmatic. I've done a very similar case exactly how you said (my patient had critical AS-was scheduled for an AVR the next day). We've all done things because it would look bad in court otherwise, even you. And I'm not convinced your way would necessarily fail the orals (obviously don't have first hand experience with the boards-but there is rarely only 1 way to provide a safe anesthetic).

As for the original patient's HR, I'd give esmolol.
 
Correct.
Because I (personally) think that he needs to avoid creating a hemodynamic disaster and then try to correct it.

This is just ridiculous. No examiner is going to fail the Jeff05/loveumms approach. It's perfectly reasonable and safe - though perhaps the ward bounce is too inefficient for the real world. I don't believe for a second that any of these allegedly young/PP examiners would fail this approach.

I'm also not 100% on board with the topicalization/propofol approach. My first thought after seeing the word "achalasia" was "huge dilated esophagus full of crap" ...

http://www.uptodate.com/online/content/images/gast_pix/Classic_achalasia_Ba_swallo.jpg
Classic_achalasia_Ba_swallo.jpg

Christ man, look at that thing; it's as big as his stomach. I'd be less worried about your hemodynamic disaster and more worried about an aspiration disaster.

I would intubate this patient.
 
😀
The good news is that you will pass your boards most likely (unless I was your oral examiner), but then you will have to relearn anesthesia if you go to private practice.

This is what I said, I did not say that I think that he would fail his exam, I said that if I were his examiner ( or a few young examiners I know personally) I would rather hear him say that he is not going to give an anesthetic that would create more risk to the patient than necessary for such a minor procedure, but I am not the examiner, I am just a simple private practice anesthesiologist.
I am not advising anyone to answer this way on the boards because they will certainly drag you to a position where the patient would aspirate or have a hemodynamic collapse or both.
So, as I said if my opinion does not appeal to you just ignore it.
 
Planktonmd said:
The good news is that you will pass your boards most likely (unless I was your oral examiner),

Planktonmd said:
By the way, you will soon find out that there are many young examiners on the oral board who share my view.

So, you would fail an examinee who took the Jeff05/loveumms approach, and you think that there are many other examiners who feel the same way. At this point in the thread, you had the strong belief that the propofol MAC was a superior anesthetic. So much so that you declared the "optimize then RSI" plan to be one that risks failure from younger, presumably more enlightened, oral board examiners.

This is what I said, I did not say that I think that he would fail his exam, I said that if I were his examiner ( or a few young examiners I know personally) I would rather hear him say that he is not going to give an anesthetic that would create more risk to the patient than necessary for such a minor procedure, but I am not the examiner, I am just a simple private practice anesthesiologist.

Now you're backtracking from "I'd fail you and many other examiners would fail you" to "I and many other examiners would prefer you did it my way" ... with the implication that there are other reasonable approaches and that maybe you (and they) wouldn't fail the examinee after all.

You're allowed to change your opinion over the course of a thread; just don't get all huffy and pretend that what you meant all along was more moderate.
 
So, you would fail an examinee who took the Jeff05/loveumms approach, and you think that there are many other examiners who feel the same way. At this point in the thread, you had the strong belief that the propofol MAC was a superior anesthetic. So much so that you declared the "optimize then RSI" plan to be one that risks failure from younger, presumably more enlightened, oral board examiners.



Now you're backtracking from "I'd fail you and many other examiners would fail you" to "I and many other examiners would prefer you did it my way" ... with the implication that there are other reasonable approaches and that maybe you (and they) wouldn't fail the examinee after all.

You're allowed to change your opinion over the course of a thread; just don't get all huffy and pretend that what you meant all along was more moderate.
You got it wrong.
I am not changing my mind or backtracking anything.
What I said is very obvious and straight forward:
This procedure does not require a general anesthetic and can be done safely the way I described.
My opinion is that doing a GA even after you optimize the patient is still more risky and not needed so it is in my opinioin WRONG!
and IF I WAS THE EXAMINER I WILL FAIL YOU IF YOU SAY THAT THIS IS THE BEST PLAN OF ACTION.
Now use your vast experience and infinite knowledge and come up with another smart ass statement.
I wish people would read and understand the posts before they start analyzing them.
 
Last edited:
Yes,
I think you should have done topical anesthesia to the throat, gave little touches of Propofol and let the GI guy empty the esophagus.


Would not have been possible. He couldn't suck out the stuff - it was chunks. Furthermore, it took an hour (and this was an experienced attending). Thats a LONG time to give someone propofol without a secure airway knowing that she is at risk of aspiration at any second if just a bit too much propofol is given.

We gave 1 of midaz and she was basically under 0.5 MAC - falling asleep quite easily. Then we gave 2 of etomidate, another 2 she was pretty sleepy at that point. Cricoid, sux then another 2 of etomidate. Maybe not 100% a RSI but, we wanted her at least a little sleepy before the sux.
 
Now use your vast experience and infinite knowledge and come up with another smart ass statement.

Ah, impugning my experience and knowledge. My feelings are hurt.

I wish people would read and understand the posts before they start analyzing them.

I read, I understand. You think GA is unsafe in this patient. And you're so dogmatic in your "only one way to do this" assessment that you think medically optimizing a patient for an elective procedure and delivering a GA is unsafe.

Inefficient, maybe. Unnecessary, maybe. These are debatable points. But unsafe?

I disagree.

And in reading this thread and seeing what actually happened (an hourlong EGD in a patient with an esophagus full of chunks) ... I'm going to continue to assert that your MAC plan carries aspiration risks that the GA plan doesn't. (Risks you haven't even acknowledged in this thread.)

But even so, I won't say your MAC approach is categorically unsafe and deserving of a board failure.

Comprende, compadre?
 
So, you think it is safer to gradually do a rapid sequence 😀 (I have to admit I've never heard of a gradual RSI before, sorry) then give Sux which will effectively abolish all the airway protective reflexes on a patient with an esophagus full of crap, then hope and pray that you can intubate before she aspirates, then maintain general anesthesia on this patient with severe aortic stenosis and unstable hemodynamics?
The only reason you are convinced it is safer is because they told you so, over and over and over.
Who is being dogmatic here?
You need to be open minded and think that what they teach you, although seems to make sense at this point of your training, might (just might) be not the best choice always!
I have a feeling that these days residents are being taught arrogance before anesthesia, this used to be an exclusive thing to surgical residencies.



Ah, impugning my experience and knowledge. My feelings are hurt.



I read, I understand. You think GA is unsafe in this patient. And you're so dogmatic in your "only one way to do this" assessment that you think medically optimizing a patient for an elective procedure and delivering a GA is unsafe.

Inefficient, maybe. Unnecessary, maybe. These are debatable points. But unsafe?

I disagree.

And in reading this thread and seeing what actually happened (an hourlong EGD in a patient with an esophagus full of chunks) ... I'm going to continue to assert that your MAC plan carries aspiration risks that the GA plan doesn't. (Risks you haven't even acknowledged in this thread.)

But even so, I won't say your MAC approach is categorically unsafe and deserving of a board failure.

Comprende, compadre?
 
We gave 1 of midaz and she was basically under 0.5 MAC - falling asleep quite easily. Then we gave 2 of etomidate, another 2 she was pretty sleepy at that point. Cricoid, sux then another 2 of etomidate. Maybe not 100% a RSI but, we wanted her at least a little sleepy before the sux.
Do you think that 6 mg of Etomidate is enough to supress the response to laryngoscopy in a patient with aortic stenosis?
 
So, you think it is safer to gradually do a rapid sequence 😀

Jeff05 said:
RSI with Etomidate/Succ. Esmolol and lidocaine IV upfront.

I said nothing about a "gradual" RSI.

I would not induce 2mg at a time. I disagree with that aspect of the way loveumms did the induction.

(I have to admit I've never heard of a gradual RSI before, sorry) then give Sux which will effectively abolish all the airway protective reflexes on a patient with an esophagus full of crap, then hope and pray that you can intubate before she aspirates, then maintain general anesthesia on this patient with severe aortic stenosis and unstable hemodynamics?

As opposed to (partially) ablating protective airway reflexes with topicalization, doing an hourlong case with an usecured airway in a patient with an esophagus full of crap, and hoping and praying that she doesn't aspirate?

Again, for all the reasons laid out by copro, I don't think this patient's hemodynamics deserve such abject GA avoiding terror, particularly after better rate control is achieved.

Rational people can discuss how the various risks in this case can best be managed. But you don't seem to be interested in that.

Planktonmd said:
I have a feeling that these days residents are being taught arrogance before anesthesia, this used to be an exclusive thing to surgical residencies.

Pot, kettle, black.

For the love of god, one of us is declaring absolute knowledge and asserting one way to do the case, and one of us is not.
 
Topical anesthesia to the oropharynx might supress the gag reflex (a good thing) but will not supress the cough reflex and the ability of the epiglottis to protect the airway.
Sux will leave you with a wide open larynx and true unprotected airway until you hopefully can intubate, and if you can't do it fast enough it will be almost certain that this patient will aspirate.
A rapid sequence induction of anesthesia is the way to go when you have to do GA on someone with full stomach but in this case YOU DON"T have to do GA, you really don't.




I said nothing about a "gradual" RSI.

I would not induce 2mg at a time. I disagree with that aspect of the way loveumms did the induction.



As opposed to (partially) ablating protective airway reflexes with topicalization, doing an hourlong case with an usecured airway in a patient with an esophagus full of crap, and hoping and praying that she doesn't aspirate?

Again, for all the reasons laid out by copro, I don't think this patient's hemodynamics deserve such abject GA avoiding terror, particularly after better rate control is achieved.

Rational people can discuss how the various risks in this case can best be managed. But you don't seem to be interested in that.



Pot, kettle, black.

For the love of god, one of us is declaring absolute knowledge and asserting one way to do the case, and one of us is not.
 
Why can't we just have a discussion without getting so defensive about what we think is right? There are many ways to do a case and two ways might be correct.

You make it seem like we titrated the etomidate over 10 minutes. We gave it slowly over 15 seconds instead of pushing it over 2 seconds because we didn't want a huge drop in blood pressure and we were unsure of how much it would take. Given her response to midaz, we knew it wouldn't take much but we were unsure. Sometimes you have to trade one risk for another.

I guess I shouldn't have called it a true RSI since we didn't push the etomidate then immediately push the sux but, we did it for a reason. I think we probably could have intubated without the sux since her posterior oropharynx was numb (and I think this is the reason that she didn't have a sympathetic response to laryngoscopy). We pushed the sux and 20 seconds later intubated her without problem.

Who knows if MAC would have worked. That was originally our plan. I'm glad we didn't do it in the end but, that is just my own opinion. Not because that's what my attendings have told me but, because I think it was safer for the patient.

Yes, it would have been awful if we would have had an aspiration up front but, if she aspirated once during a MAC we would have had to intubate her to prevent further aspirations and at that point it would have been a STAT intubation since she likely would have become hypoxic (worsening her oxygen delivery) and it would have likely resulted in much greater hemodynamic derangements.

I don't think I ever said her hemodynamics were unstable. Yes, she was tachycardic but, her BP was stable and she was tolerating the tachycardia.

To answer the earlier question about etomidate and adrenal suppression. We gave her stress steroids 10 minutes before going back to the endo suite. She had been on 5mg of prednisone for many years for the lupus.

I think it's funny that everyone is so wrapped up in the "correct" oral board answer because the attending that tooj over the case is an oral board examiner. He didn't have any problems with the plan.
 
Yes, because it did. Every patient is different.

OK,
By the way if you guys thought that the esophagus was so full of stuff and you really wanted to do GA, did you consider that maybe it would have been a good idea to place an NG tube first and decompress the esophagus as much as possible before induction?
 
OK,
By the way if you guys thought that the esophagus was so full of stuff and you really wanted to do GA, did you consider that maybe it would have been a good idea to place an NG tube first and decompress the esophagus as much as possible before induction?


No, we didn't although we probably should have. Might have done it however, most of what she had in her esophagus was not going to be removed with an NGT. It really was small chunks of food with a barium coating (a little smaller than pea sized).

Another reason I forgot to mention regarding why I'm glad we did GA. To get the barium and chunks out, the GI doc had to do a crap load of irrigation. He thought it would just be pushed through after dilation of the stricture but, that didn't happen as planned.
 
Topical anesthesia to the oropharynx might supress the gag reflex (a good thing) but will not supress the cough reflex and the ability of the epiglottis to protect the airway.

Your points are well taken, but a patient who's sedated enough and topicalized enough to tolerate a big pipe being shoved down his throat does not have normal airway reflexes. There's a risk of aspiration no matter what approach you take. A MAC exposes the patient to the risk for the duration of the case. Assuming no red flags suggesting a difficult intubation, a RSI minimizes the time the patient is exposed to that risk.

RSI isn't without its own risks, including shortcomings specific to this patient. Eg, cricoid pressure in this patient would be utterly useless, given how dilated the esophagus is likely to be at that level. So as you point out, you're relying on the R part of the RSI.

We do GAs on patients with AS all the time, and they survive. In this patient, who's alive and asymptomatic with a HR in the 120s, I am not fearful of his AS. Cognizant of the issue and attentive to keeping his hemodynamics in the box, yes ... hell bent on avoiding GA, no.

Finally, I think it's a fallacy to simply assume that a propofol/MAC technique will allow you to totally sidestep hemodynamic issues. A touch of hypotension from your sedation, a touch of vagal stimulation from the procedure, and now you're managing some of the same issues ... except here you have a prone patient with an unsecured airway complicating things.
 
Nasty drug with bad side effects like nausea, vomiting and adrenal depression. Many believe AD only happens with repeat doses but I have seen it with one dose only.

To get back to an earlier part of the thread, I had this same discussion with some other residents a couple weeks ago. Some argued that suppression after a single dose is theory without much clinical significance.

I think it's worth mentioning that the board agrees that one dose is enough to cause adrenal suppression. It was specifically tested in 1990 and I'm pretty sure it was on the ITE a couple years ago or maybe one of the AKTs (I remember having the same conversation about one-dose adrenal suppression early in residency after one of those tests).

1990 ITE Book A said:
19. A single dose of etomidate for induction of anesthesia will cause
(A) adrenal cortical suppression
(B) decreased skeletal muscle tone
(C) hypotension
(D) increased airway reactivity
(E) tachycardia

key: A
 
To get back to an earlier part of the thread, I had this same discussion with some other residents a couple weeks ago. Some argued that suppression after a single dose is theory without much clinical significance.

I think it's worth mentioning that the board agrees that one dose is enough to cause adrenal suppression. It was specifically tested in 1990 and I'm pretty sure it was on the ITE a couple years ago or maybe one of the AKTs (I remember having the same conversation about one-dose adrenal suppression early in residency after one of those tests).

Interesting. We use etomidate quite a bit in the peds ER. RSI or even just sedation for a CT where something fast with a short half life is needed. In general I've not seen any cases of adrenal suppression for those kinds of things, however a recent case was admitted to the PICU that raised questions about the drug. 1 year old girl intubated in the ER (etomidate and roc) for severe respiratory distress turned out to have strep pneumo sepsis. White count upstairs the next day was 0.7 and needed pressors. I attribute all of that to being septic, but some questioned whether the etomidate affected her adversely.

Still the only case where the question even came up in the past four years.
 
Interesting. We use etomidate quite a bit in the peds ER. RSI or even just sedation for a CT where something fast with a short half life is needed. In general I've not seen any cases of adrenal suppression for those kinds of things, however a recent case was admitted to the PICU that raised questions about the drug. 1 year old girl intubated in the ER (etomidate and roc) for severe respiratory distress turned out to have strep pneumo sepsis. White count upstairs the next day was 0.7 and needed pressors. I attribute all of that to being septic, but some questioned whether the etomidate affected her adversely.

Still the only case where the question even came up in the past four years.

Adrenal suppression doesn't explain the neutropenia. She probably had some inborn immune deficiency.

To tie these together, as few weeks ago ortho added on an radial ORIF. Pt had eaten ~4 hours before, so the case just got moved to the last of the day for NPO reasons. I saw her as the PACU resident (boarding in holding). Flipping through her chart, I noticed the ER had reduced her fracture with: 150mcg of fentanyl, 4mg of midazolam and 10 mg of etomidate. Essentially an induction. I thought it ironic given that we were sitting on her waiting for the magical 8 hours.
 
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