Anesthesia Dogma

[Ignatius J]

http://www.saj.med.br/uploaded/File/Increased Long Term Mortality After a High.pdf

First do no harm. Perhaps, a high Fio2 is detrimental to our sickest patients undergoing surgery?

Definitely not advocating a singular way to do everything. Obviously, each patient needs consideration for a tailored anesthetic. But in a case with restricted access to the airway such as a prone crani in pins (have seen a lost airway with this before and it was not pretty), I don't think maintaining on .9-.95 is "doing harm". We can argue the positives and negatives, but in the end, we are physicians and must decide what is best on a case by case basis. My only point is that folks generalize about 100% being detrimental to patients. And that's simply a generalization, not to be confused with a standard of care.

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[IlDestriero]

I think that high oxygen absolutely causes atelectasis, that is without question, and thinking that a few recruitment breaths will reverse it is optimistic. I had a dunce surgeon get cute with the drapes and extubate a pt in pins prone and 180 after a 6-8 hour marathon. I got down on the floor and reintubated him upside down and backwards while the surgeon scowled at himself and the nurse called for help. It was surprisingly easy BTW. After that experience do I do anything different? No. I tape the tube in properly, secure it well and use 40% O2.
Doing something that the literature suggests might be dangerous and that you know causes atelectasis is a questionable decision based on the fear of what should be an extremely rare event. I wake up on 80% 99% of the time as well. I watch the residents crank the O2 to 10 L for extubation and cringe every time.

 

[IanMcGalt]

N

 

[urge]

I had a dunce surgeon get cute with the drapes and extubate a pt in pins prone and 180 after a 6-8 hour marathon. I got down on the floor and reintubated him upside down and backwards while the surgeon scowled at himself and the nurse called for help. It was surprisingly easy BTW.

I want to hear more about it. Same blade as when the case started? Did you alter the position of the head? How much saliva hit your eyes?

My reaction would have been to put an LMA.

 

[Planktonmd]

Exactly... I have been there too and LMA was the answer

 

[Ignatius J]

I think that high oxygen absolutely causes atelectasis, that is without question, and thinking that a few recruitment breaths will reverse it is optimistic. I had a dunce surgeon get cute with the drapes and extubate a pt in pins prone and 180 after a 6-8 hour marathon. I got down on the floor and reintubated him upside down and backwards while the surgeon scowled at himself and the nurse called for help. It was surprisingly easy BTW. After that experience do I do anything different? No. I tape the tube in properly, secure it well and use 40% O2.
Doing something that the literature suggests might be dangerous and that you know causes atelectasis is a questionable decision based on the fear of what should be an extremely rare event. I wake up on 80% 99% of the time as well. I watch the residents crank the O2 to 10 L for extubation and cringe every time.

I don't agree that the literature says it is dangerous. I think evidence is conflicting at best. If you are saying matter-of-factly that high Fi02 is dangerous for all patients, then you are just cherry-picking from the literature for the sake of convenience. That's how dogma perpetuates itself.

 

[nimbus]

Alveolar recruitment maneuvers DO work. Directly observed this on a routine basis during heart and lung cases. And even without direct observation, it is clinically effective. Also, after an hour or more when all the compartments are at steady state, is absorption atelectasis still an issue?

 

[Ignatius J]

Alveolar recruitment maneuvers DO work. Directly observed this on a routine basis during heart and lung cases. And even without direct observation, it is clinically effective. Also, after an hour or more when all the compartments are at steady state, is absorption atelectasis still an issue?

If you have an arterial line, it's pretty interesting to see atelectasis in real time based on the P/F ratio before and after induction. General anesthesia causes a buttload of atelectasis in and of itself, but here we are beating up on Fi02. Quite ironic when someone won't even consider an epidural for an ex lap/bowel resection to help curtail post-op pulmonary complications among pain and other things, or maybe regional in an ortho case, but by God, don't you dare put that patient on 100% upon extubation!

 

[IlDestriero]

Here's what I said. You are suggesting that I said something completely different and then waving the dogma flag.

I think that high oxygen absolutely causes atelectasis, that is without question, and thinking that a few recruitment breaths will reverse it is optimistic.

Doing something that the literature suggests might be dangerous and that you know causes atelectasis is a questionable decision based on the fear of what should be an extremely rare event.

And I agree that lung recruitment does recruit alveoli and improve atelectatic lung tissue BUT I doubt that 1. Most do it correctly or enough or even at all, and 2. I doubt that even if done correctly, it effectively recruits all/most of the alveoli that you lost due to completely avoidable absorption atelectasis from unnecessary prolonged high O2 in addition to the usual post anesthesia/vent atelectasis.
There are studies showing 100% O2 at emergence causes significant atelectasis in just that short time, I'm not aware of any showing that a couple 30 for 30 breaths completely reverses it.

 

[Ignatius J]

Here's what I said. You are suggesting that I said something completely different and then waving the dogma flag.



And I agree that lung recruitment does recruit alveoli and improve atelectatic lung tissue BUT I doubt that 1. Most do it correctly or enough or even at all, and 2. I doubt that even if done correctly, it effectively recruits all/most of the alveoli that you lost due to completely avoidable absorption atelectasis from unnecessary prolonged high O2 in addition to the usual post anesthesia/vent atelectasis.
There are studies showing 100% O2 at emergence causes significant atelectasis in just that short time, I'm not aware of any showing that a couple 30 for 30 breaths completely reverses it.

Is atelectasis the endpoint of the argument? Or are adverse outcomes affecting morbidity? I would intuitively argue that not waking the patient up on 100% leads to increased incidences of desaturations with bronchospasm or post-extubation largyngospasm/obstruction, but it would foolish to say that it affected morbidity. Just using "atelectasis" as the buzzword does not say anything about patient outcome.

 

[pgg]

I give just about everybody 4mg of dexamethasone with induction. It has good antiemetic and analgesic effects, with a great risk profile. I'm curious why urge would not want it.

 

[urge]

I give just about everybody 4mg of dexamethasone with induction. It has good antiemetic and analgesic effects, with a great risk profile. I'm curious why urge would not want it.

Altered wound healing and impaired immune system vs nausea? I'll take the nausea for 500.