Awake FOB not being used as much?

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I refrained from posting the same thing as pgg because you could potentially get a faster wake up due to redistribution to the fat compartment...?

I don't know, I bet the fat would work against you there too, as it gradually releases its agent back into the blood while you're trying to wake up.
 
Sorry to add something not related to the corollary, but it needs to be added.

The

BOUGIE

Has changed our business.

Also called the Eschman,

and I'm sure I spelled it wrong.

Being able to visualize just enough but not enough to pass an endotracheal tube but enough to pass a stylette like thinghy and then Seldinger the tube over the stylette

reduced the fiberoptic need by about 99%.

Totally agree Jet. We are taught that part of our morning setup includes always making sure you have a LMA 3,4,5 available in the room. I now routinely make sure I have a bougie too. There are times I could of totally avoided abandoning laryngoscopy to reventilate before retrying if I had the bougie readily available. It makes a world of difference, even in the case you don't see cords but see a hint of arytenoid. Feeling those tracheal ring clicks is a great feeling.

Once I had a case go sour and even glidescope provided inadequate view. Used the power of the bougie with the glidescope and hit it right away. Saved my *****.
 
I don't know, I bet the fat would work against you there too, as it gradually releases its agent back into the blood while you're trying to wake up.

Maybe in a 4 hour sevo case, but I doubt it would have much effect during a quick induction .
 
You could well be right. I'm just extrapolating the dramatically increasing inhalation induction times for kids -> adolescents -> adults, and adding in -> obese adults at the end. That may not be justifiable; I don't have a counter argument to your convincing FA/Fi curve and tissue groups.


Wouldn't something like CO have a much more profound effect on onset than fat?
 
Totally agree Jet. We are taught that part of our morning setup includes always making sure you have a LMA 3,4,5 available in the room. I now routinely make sure I have a bougie too. There are times I could of totally avoided abandoning laryngoscopy to reventilate before retrying if I had the bougie readily available. It makes a world of difference, even in the case you don't see cords but see a hint of arytenoid. Feeling those tracheal ring clicks is a great feeling.

Once I had a case go sour and even glidescope provided inadequate view. Used the power of the bougie with the glidescope and hit it right away. Saved my *****.


So you can't see squat, and reach for the bougie. It feels OK, and you slide the ETT down it, but unfortunately it's in the goose. So now, do you:

1. leave the goosed tube in situ, and re-bougie, or

2. remove the tube from the gus, and start from scratch with another bougie attempt?
 
Especially in stupendously obese people - it's going to take f o r e v e r to get them deep enough to do anything, and maintaining SV doesn't mean they won't obstruct the way they always do when they go to sleep in their beds at home.


really? clearly a gas induction isn't a good idea in the gargantuan, and clearly wake-up is slower from saturation of the large fat compartment, but - is onset of anesthesia delayed in the morbidly obese with volatile anesthesia? I ask because I don't know the answer, and can't find any clinical evidence.

uptake into the fat group is increased with the size of the compartment, which delays equilibration, and wake-up, but i believe the slope and height of the steep part of the FA/Fi curve to be due primarily to - first - solubility of the gas in blood and - second - saturation of the vessel-rich group. The flatter, later part of the curve is influenced more by saturation of - third- the muscle group, and -fourth - the fat group (and the fingernails are negligible).

I wager that the onset of clinical anesthesia is not significantly different in the morbidly obese with volatile anesthesia. If I'm wrong, I would love to see the clinical studies and justification.

an increased cardiac output in this population could delay inhalation induction
 
an increased cardiac output in this population could delay inhalation induction

right, it could, but they also have a decreased FRC (which would speed induction), and the increased CO goes to... fat. and the body fat (percentage) doesn't contribute (much) to the onset of clinical anesthesia - this is more a function of solubility, and equilibrium with the vessel-rich group.

all this being said, the study hasn't been done so far as i am aware...
 
right, it could, but they also have a decreased FRC (which would speed induction), and the increased CO goes to... fat. and the body fat (percentage) doesn't contribute (much) to the onset of clinical anesthesia - this is more a function of solubility, and equilibrium with the vessel-rich group.

all this being said, the study hasn't been done so far as i am aware...

It doesn't matter that the increased CO goes to fat, increased cardiac output -> increased uptake of anesthestic -> decreased partial pressure = slowed induction. Whether the prolongation is clinically significant is another story.
 
right, it could, but they also have a decreased FRC (which would speed induction), and the increased CO goes to... fat. and the body fat (percentage) doesn't contribute (much) to the onset of clinical anesthesia - this is more a function of solubility, and equilibrium with the vessel-rich group.

all this being said, the study hasn't been done so far as i am aware...

Increased CO delays inhalation inductions because it reduces the concentration of dissolved agent in blood leaving the heart. This phenomenon is not dependent upon body fat %.

I don't know how clinically significant that is, but my gut feeling (for all that's worth 🙂) is that morbidly obese patients do have slower inhalation inductions and this seems like a good reason why. Of course I realize I'm starting with the result I expect and looking for data and reasons to support it ...


ETA - GypsySongman beat me to it, that's what I get for having 9 windows open and answering one at a time without checking the threads again first 🙂
 
It doesn't matter that the increased CO goes to fat, increased cardiac output -> increased uptake of anesthestic -> decreased partial pressure = slowed induction. Whether the prolongation is clinically significant is another story.

correct. i didn't intend to imply that it matters where the increased cardiac output goes, only that the increased CO in the morbidly obese is insignificant insofar as onset of volatile anesthesia is concerned. (In addition most of the truly morbidly obese have an increase in CO that is limited by cardiomyopathy and pHTN.) More important is the slope and height of the FA/Fi curve, which again is dependent on solubility and equilibrium in the vessel rich group.

even if there was an increase in CO this factor is less significant with the far less soluble agents we use today - this was a more pertinent part of the equation in the days of halothane...
 
2 interesting papers on the subject. eger and friends put a baby whale to sleep and plotted the FA/Fi curves (that older paper is with highly soluble agents) - the paper has a great picture. EZ MBV - mask blowhole ventilation. the first paper is likely more valid and applicable, but the second one is definitely more fun.

bottom line - with the less soluble anesthetics, onset of anesthesia ie wash-in is likely not significantly affected by BMI (blubber-mass-index).

Obesity Modestly Affects Inhaled Anesthetic Kinetics in Humans

  1. <LI class=contributor id=contrib-1>Hendrikus J. M. Lemmens, MD, PhD*, <LI class=contributor id=contrib-2>Lawrence J. Saidman, MD*, <LI class=contributor id=contrib-3>Edmond I. Eger II, MD† and
  2. Michael J. Laster, DVM†
Anesthetic uptake--of mice and men (and whales).
Wahrenbrock EA, Eger EI 2nd, Laravuso RB, Maruschak G.
 
We rotate through two major hospitals at my program--one is a level I trauma center, one is a quaternary care type academic hospital. Awake FOIs are mostly reserved for head and face trauma at the first hospital (of which there is an over-abundance) and complex head and neck cancers at the second hospital (not nearly as many as the trauma hospital, but still a great deal).

I went almost a year without ever doing an awake FOI when I was doing my subspecialty rotations. I do believe most procedures are like riding a bicycle in that once you get the hang of it, a certain amount of muscle memory sets in and you can not do the procedure for a long time and still be okay.

But when a resident finishing their CA-1 tells me they've only done three, well, that's not like riding a bike. The key to getting good at something is doing it many times in a short time period.

I do believe we are not doing as many awake FOIs as we used to which is probably not a good thing. Anyone with grossly abnormal airway anatomy (not necessarily obesity per se but trauma and the ENT cancer patient) is has too high of a chance of being in the unable to intubate, unable to ventilate category. Obviously each patient needs to be approached individually, but if your practice is likely to include the above type of patient, I think it behooves you to get more awake FOIs under your belt.

You do not want to be on call by yourself at night dealing with one of these patients when you don't feel comfortable with your awake FOI skills. I don't care if you're not the best at blocks or IVs or epidurals, etc. No one died from not having a block. Airway is a different story.
 
I dont do many ENT extreme cases, but in 2 years of PP i have not used an AFOI. Glidescope all the way, have done multiple ICU intubations on 300kg pts without struggle.
Two whole years huh? No offense but the lack of a problem in thy time frame is proof of nothing.
 
patient refuses

patient doesnt tolerate

"a little" sedation turns into snoring followed by laryngospasm/bronchospasm


Patient refusal hasn't ever happened to me in this situation in 20 years with a clear risk explanation.
Patient doesnt tolerate almost did once (I finally got I in) but I am better at topical etc than I was then.
I once oversedated an awake fiberoptics and almost lost them...I was an ass for trying a new sedation technique on that patient. I have not seen sedation progress to laryngospasm. I'm not quite sure how that would happen.
 
Patient refusal hasn't ever happened to me in this situation in 20 years with a clear risk explanation.
Patient doesnt tolerate almost did once (I finally got I in) but I am better at topical etc than I was then.
I once oversedated an awake fiberoptics and almost lost them...I was an ass for trying a new sedation technique on that patient. I have not seen sedation progress to laryngospasm. I'm not quite sure how that would happen.

I think that sedation can easily progress to obstruction rather than laryngospasm.
 
I've done it in a post radiation neck surgery patient and it worked great. She was skinny and would have been easy to ventilate.
I would not use this technique in an obese patient.

post radiation patients are ALWAYS awake fiberoptics.
doesn't matter how skinny they are they are often difficult to ventilate.
 
Patient refusal hasn't ever happened to me in this situation in 20 years with a clear risk explanation.
Patient doesnt tolerate almost did once (I finally got I in) but I am better at topical etc than I was then.
I once oversedated an awake fiberoptics and almost lost them...I was an ass for trying a new sedation technique on that patient. I have not seen sedation progress to laryngospasm. I'm not quite sure how that would happen.

get a patient a little too sedated and then touch their cords. im not saying its common, just something ive seen
 
post radiation patients are ALWAYS awake fiberoptics.
doesn't matter how skinny they are they are often difficult to ventilate.

I agree with Jeff. This is a great pearl. You can be led into a false sense of security with the skinnies that have had radiation to the neck.

Spider sense always goes off when I hear radiation to the neck.

I've seen some people get their heads ripped off by senior/silverback attendings at my old training institution due to the fact that they did not appreciate the significance of this. One of them got burned, only to be bailed out via a surgical AW.

CT is helpful to determine Awake vs. asleep + SV (which is always more risky and sometimes more difficult due to inadequate sedation/preperation/patient cooperation/too deep of sedation leading to obstruction).
 
For those of you in the Team Model.... another option for difficult fiberoptic intubation is a combined glidescope/fiberoptic intubation. It is a 2 man technique, but it works pretty well if you are having trouble getting to the cords with the fiberoptic scope.

Place the black snake infront of the vocal cords or whatever structure looks to be the highway to the vocal cords. This part is done under direct visualization with glidescope. Then, drive the snake into the hole via the bronchoscope.
 
post radiation patients are ALWAYS awake fiberoptics.
doesn't matter how skinny they are they are often difficult to ventilate.

We've probably all seen the post radiation difficult intubation, but I've yet to see the difficult to ventilate. I've noticed that they get fibrosed open with a patent airway that doesn't collapse.
 
We've probably all seen the post radiation difficult intubation, but I've yet to see the difficult to ventilate. I've noticed that they get fibrosed open with a patent airway that doesn't collapse.

I have seen more than one that wasn't difficult. It was impossible.
 
For those of you in the Team Model.... another option for difficult fiberoptic intubation is a combined glidescope/fiberoptic intubation. It is a 2 man technique, but it works pretty well if you are having trouble getting to the cords with the fiberoptic scope.

Place the black snake infront of the vocal cords or whatever structure looks to be the highway to the vocal cords. This part is done under direct visualization with glidescope. Then, drive the snake into the hole via the bronchoscope.

YES. also works well for suboptimal glidescope view where you can see some cords but cannot get the tube anterior enough.
 
idiot proof anaesthesia for fatties

0.05mg/kg Midazolam bolus (400lb gorilla - 8mg Midaz)
Remifentanyl TCI effect site conc 2.0ug/ml

Keep spontaneously breathing in optimal intubation position

1.2mg/kg Rocuronium, 40mg Propofol, wait 30s, laryngoscope, tube, propofol bolus, carry on

failed laryngoscopy, BMW, PLMA/ILMA, - try again

failed BMV - withdraw,

cease Remi, 16mg/kg sugammadex, 200ug Naloxone, .4mg Flumazenil. Patient awake in 2 minutes.

Then consider awake/semi sedate spont breathing fibreoptic/spinal.

What do people think?
 
idiot proof anaesthesia for fatties

0.05mg/kg Midazolam bolus (400lb gorilla - 8mg Midaz)
Remifentanyl TCI effect site conc 2.0ug/ml

Keep spontaneously breathing in optimal intubation position

1.2mg/kg Rocuronium, 40mg Propofol, wait 30s, laryngoscope, tube, propofol bolus, carry on

failed laryngoscopy, BMW, PLMA/ILMA, - try again

failed BMV - withdraw,

cease Remi, 16mg/kg sugammadex, 200ug Naloxone, .4mg Flumazenil. Patient awake in 2 minutes.

Then consider awake/semi sedate spont breathing fibreoptic/spinal.

What do people think?

Where can you get sugammadex? 😕
 
cease Remi, 16mg/kg sugammadex, 200ug Naloxone, .4mg Flumazenil. Patient awake in 2 minutes.

Talk about a hangover.... Curious, does anyone know if you you reuse the aminosteroidal NMB after sugammadex is given? I have no experience with that drug.
 
Where can you get sugammadex? 😕

nowhere in the US unless the patient is participating in a study. And I'm guessing anybody that would benefit from it with an iffy airway has probably already been excluded from the study for other reasons (morbid obesity).
 
Curious, does anyone know if you you reuse the aminosteroidal NMB after sugammadex is given? I have no experience with that drug.

I've never used Sugammadex, but my undestanding is that it has affinity for all the steroid NMBDs, though to somewhat varying degrees. Redosing a steroid NMDB probably isn't going to have the expected effect. If redosing of relaxant is desired later, the benzylisoquinoliniums will work as normal though.
 
idiot proof anaesthesia for fatties

0.05mg/kg Midazolam bolus (400lb gorilla - 8mg Midaz)
Remifentanyl TCI effect site conc 2.0ug/ml

Keep spontaneously breathing in optimal intubation position

1.2mg/kg Rocuronium, 40mg Propofol, wait 30s, laryngoscope, tube, propofol bolus, carry on

failed laryngoscopy, BMW, PLMA/ILMA, - try again

failed BMV - withdraw,

cease Remi, 16mg/kg sugammadex, 200ug Naloxone, .4mg Flumazenil. Patient awake in 2 minutes.

Then consider awake/semi sedate spont breathing fibreoptic/spinal.

What do people think?

i think your patient arrests before your reversal drugs have a chance to effect change. if you fail laryngoscopy and fail BMV thats at least 60 seconds down and your sats are probably in the low 90s/high 80s. ive also never seen sugammadex so ill have to take your word for it that it can reverse high dose roc blockade in under 2 minutes
 
idiot-proof or idiotic?😛😎🙂

I think that this is a recipe for disaster.

If you are going to this much trouble just do it awake.

idiot proof anaesthesia for fatties

0.05mg/kg Midazolam bolus (400lb gorilla - 8mg Midaz)
Remifentanyl TCI effect site conc 2.0ug/ml

Keep spontaneously breathing in optimal intubation position

1.2mg/kg Rocuronium, 40mg Propofol, wait 30s, laryngoscope, tube, propofol bolus, carry on

failed laryngoscopy, BMW, PLMA/ILMA, - try again

failed BMV - withdraw,

cease Remi, 16mg/kg sugammadex, 200ug Naloxone, .4mg Flumazenil. Patient awake in 2 minutes.

Then consider awake/semi sedate spont breathing fibreoptic/spinal.

What do people think?
 
Why? How did the airway get obstructed? Tracheal issue like sevo suggested?

Obstruction that is impossible to alleviate.

I am talking about the crusty old dudes that look and feel like a nuclear weapon exploded on their face and neck. No landmarks on a neck that is hard as a rock, inability to open the mouth more than a cm or so, neck fused in place and unable to extend at all and jaw frozen in place. Intraoral pathology may also work against you such as redundant, fibrotic scarred tissue and probably tracheal narrowing as well.

I think that relaxation of the soft tissues combined with all of the above can make for a disaster.
 
idiot proof anaesthesia for fatties

0.05mg/kg Midazolam bolus (400lb gorilla - 8mg Midaz)

[...]

What do people think?

I think 400 pounds = 182 kg = 9.1 mg midaz per that formula, but that's splitting hairs.

What I really think is that 8 mg of midazolam is an induction dose all by itself in an awful lot of people, especially the fat OSA population.
 
numerous landmark studies which show inadequate relaxation to be the cause of difficult BMV. paralysing someone adequately allows for the best possible conditions for intubation. 16mg/kg of sugammadex will reliably result in return of TOF within 30s of IV administration following 1.2mg/kg dose of Rocuronium. Works every time. Without fail. Much faster than wear off time for suxamethonium. Expensive though. Looking at $3000 dose of Sugammadex.
Benefit of doing Midaz and Remi is to minimise incidence of awareness while also using agents which have IV antidotes as opposed to Sevo/Propofol which once given, rely on redistribution for their offset.
 
one of my faves for airway badness:
glidescope with the fiberoptic scope locked and loaded and ready to be used as a flexible, maneuverible bougie with visualization
This has bailed me out of a few close calls
 
numerous landmark studies which show inadequate relaxation to be the cause of difficult BMV. paralysing someone adequately allows for the best possible conditions for intubation. 16mg/kg of sugammadex will reliably result in return of TOF within 30s of IV administration following 1.2mg/kg dose of Rocuronium. Works every time. Without fail. Much faster than wear off time for suxamethonium. Expensive though. Looking at $3000 dose of Sugammadex.
Benefit of doing Midaz and Remi is to minimise incidence of awareness while also using agents which have IV antidotes as opposed to Sevo/Propofol which once given, rely on redistribution for their offset.

Suggamadex, if it was available and inexpensive, would probably change the way I do RSIs. I think I'd never touch succinylcholine again.

I'm not so sure it would revolutionize the way I do anything else.


Also, what exactly does this mean?
ALTorGT said:
Remifentanyl TCI effect site conc 2.0ug/ml
 
Really? I wasn't aware of that

Yep. I have an attending who used them a lot in Canada for patient care and research...they sound pretty slick. Alas, the FDA doesn't like something about them.

There was a spate of letters in the March 2011 issue of Anesthesiology about their validity in research. Kind of interesting to read...the first letter was titled "Presenting Data versus Predictions as Basic Scientific Information: Target-controlled Infusions versus Microgram per Kilogram per Minutes"
 
The pre-programmed pumps are not available, but you can get programs to calculate infusion rates to manually program into your pumps for TCI.

I looked into it for a while, but ultimately decided that with enough experience, clinical judgement on infusion rates gets me close enough and is actually fairly close to what the TCI calculations would predict.

- pod
 
And of course...the blind nasal intubation.
A beautiful lost art.

Insightful point, along with eschmann post. IMO, in these days of VAL, if reaching for the FOB is a secondary or tertiary thought, you've mis-assessed the situation. If you even pick it up, it should have been your first choice. Were it not for DLT placements, I wouldn't remember the last time I put it to use.
 
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