Deep Extubation on Abdominal Cases

[pgg]

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Stage 2 does not exist.

What would you prefer to call the period of time frequently observed prior to emergence (or just after an inhalation induction), characterized by such physical signs as tachycardia, disconjugate gaze, breath holding, etc? Is it just coincidence that if one rubs the trachea with a plastic balloon and tube at this time, but typically not before or after it, that the incidence of laryngospasm is quite high?

 

[Ignatius J]

What would you prefer to call the period of time frequently observed prior to emergence (or just after an inhalation induction), characterized by such physical signs as tachycardia, disconjugate gaze, breath holding, etc? Is it just coincidence that if one rubs the trachea with a plastic balloon and tube at this time, but typically not before or after it, that the incidence of laryngospasm is quite high?

A period in the continuum (that doesn't always present itself), characterized by a recovery of excitatory neurons that have not been blunted by other pharmacological means but inadequate recovery of inhibitory neurons.

When you have a "smooth emergence", does the patient go through stage 2?

 

[IlDestriero]

I extubate deep all the time. Tubes and LMAs. To me, deep means not responding to significant stimulation, like suctioning the airway. I usually do it between 0.5 and 1 MAC of agent with appropriate opiate on board. If I'm worried about an airway, reactivity, URIs, etc. I extubate awake or at ~0.5 Mac and they're usually awake by the time I'm done in the PACU.
I would do it for abdominal cases assuming there weren't contraindications like significant reflux, risk of full stomach, etc. I don't assume that just because the OG tube didn't have any more return that they have an empty stomach. We've all seen patients that we suctioned go on to vomit significant gastric contents during emergence or in the PACU at drop off.

 

[epidural man]

Please explain the neurophysiology behind "stage 2".

I don't know about Arch, but I certainly can't explain it - but doesn't mean it isn't complicated and doesn't exist.

For my Master's thesis, I wrote on the use of Coherent-AntiStokes-RAMAN-Spectroscopy and characterization of CH3-CL3 radiofrequency induced plasmas commonly used in the etching process of computer chips. I use to understand that and could explain it - now I have no idea - doesn't mean it didn't work though.

 

[Ignatius J]

Also, I wonder - if sympathetic discharge is the issue - can we treat or even prevent laryngospasm with labetolol?

I don't think beta blockers act centrally. But a drug that has the same effect profile, like an alpha agonist (precedex), yes.

 

[Ignatius J]

I'm not disagreeing with you nor agreeing with you.

It's an interesting thought.

However...Stages have also been studied and seemed to have been replicated with the newer agents (in the abscence of polypharmacy).

Sympathetic discharge from surgical stimulis is not the same neurological phenomenon that creates laryngospasm. I think they are two distinct neurological processes and may not be on a continum as you suggest.

I would need to read these studies. I would also argue that sympathetic discharge is exactly what creates laryngospasm as evidenced by bucking at skin closure (lower gas and more pain receptor stimulation) despite a patient at 0.6 MAC being perfectly fine when closing fascia. The sympathetic discharge surges in the face of lack of recovery of inhibitory neurons (why a patient gets "disinhibited" as they go to sleep too or an every day example is why people "relax" after versed or a drink of alcohol) causing increased muscle tone, especially when someone has a tube stimulating the crap out of them.

 

[deleted162650]

I think you guys are just arguing over semantics here. Everyone seems to be in agreement that you go through a hyper-excitatory phase during both induction and emergence. Historically this has been given the name "stage 2." Yes you can significantly attenuate it with the use of narcotics or other agents. My hunch is that the brain still goes through the same process but the physical manifestations are reduced/eliminated by the narcs, etc. I have no proof to support that hypothesis though. Ignatius has nicely outlined the neurophysiology. He doesn't like the term "stage 2". OK whatever, he can call it whatever he wants. Moving on. . .

 

[epidural man]

I think you guys are just arguing over semantics here. Everyone seems to be in agreement that you go through a hyper-excitatory phase during both induction and emergence. Historically this has been given the name "stage 2." Yes you can significantly attenuate it with the use of narcotics or other agents. My hunch is that the brain still goes through the same process but the physical manifestations are reduced/eliminated by the narcs, etc. I have no proof to support that hypothesis though. Ignatius has nicely outlined the neurophysiology. He doesn't like the term "stage 2". OK whatever, he can call it whatever he wants. Moving on. . .

He isn't arguing that there is a state that is hyper-excitatory. He is arguing that there isn't a state period.

 

[Ignatius J]

He isn't arguing that there is a state that is hyper-excitatory. He is arguing that there isn't a state period.

Incorrect. It's not a "stage" because it doesn't present itself in a step-wise fashion for every anesthetic. "State" is a subjective term. Of, course with inhibited inhibitory neurons I think you are in a "hyper-excitatory state." That doesn't mean it's a "stage" that every anesthetized person goes through.

Put an LMA in a patient, titrate in fentanyl to a RR of 8, and turn the gas off. Tell me when "stage 2" presents itself.

 

[IlDestriero]

What's in a name? That which we call a rose By any other name would cause sweet laryngospasm.

 

[deleted162650]

Put an LMA in a patient, titrate in fentanyl to a RR of 8, and turn the gas off. Tell me when "stage 2" presents itself.

When the eyes are divergent.

I agree with you that the term "stage 2" is somewhat antiquated but that the hyper-excitatory state still happens as you emerge from a volatile anesthetic and yes you can significantly blunt the downstream physiologic effects with narcs to the point of them being essentially insignificant but I still think the brain goes through the same process with or without the narcs.

Now we officially sound like a bunch of Ivory tower academics in the middle of a big mental circle jerk.

 

[epidural man]

I just tried to find Stages listed in Big Miller. I couldn't find a single discussion of it...perhaps it is old news.

There was a chart that showed the 3 phases - and it said you could extubate in phase 2 or 3. The chart was from this publications

http://www.nejm.org/doi/full/10.1056/nejmra0808281

Great chapter with lots of pertinent info about what we are talking about (attached).

 

[deleted171991]

http://www.wikiwand.com/en/Guedel's_classification

http://www.wikiwand.com/en/General_anaesthesia#/Stages_of_anaesthesia

The important thing to remember is that these stages were described with inhalational agents used alone. @Ignatius J is right when saying that we might not see a full-blown stage 2 when we mix in other agents, such as opiates. Or if we use TIVA.

 

[deleted171991]

I just tried to find Stages listed in Big Miller. I couldn't find a single discussion of it...perhaps it is old news.

There was a chart that showed the 3 phases - and it said you could extubate in phase 2 or 3. The chart was from this publications

http://www.nejm.org/doi/full/10.1056/nejmra0808281

Great chapter with lots of pertinent info about what we are talking about (attached).

What is interesting is that Miller says that extubation is possible also in Phase 2 of emergence, what some would call almost awake. 😉

Emergence, Phase 1
Cessation of anesthetic drugs
Reversal of peripheral-muscle relaxation (akinesis)
Transition from apnea to irregular breathing to regular breathing
Increased alpha and beta activity on EEG

Emergence, Phase 2
Increased heart rate and blood pressure
Return of autonomic responsiveness
Responsiveness to painful stimulation
Salivation (CN VII and IX nuclei)
Tearing (CN VII nuclei)
Grimacing (CN V and VII nuclei)
Swallowing, gagging, coughing (CN IX and X nuclei)
Return of muscle tone (spinal cord, reticulospinal tract, basal ganglia, and primary motor tracts)
Defensive posturing
Further increase in alpha and beta activity on EEG
Extubation possible

Emergence, Phase 3
Eye opening
Responses to some oral commands
Awake patterns on EEG
Extubation possible

 

[epidural man]

What is interesting is that Miller says that extubation is possible also in Phase 2 of emergence, what some would call almost awake. 😉

I thought that whole chapter was very interesting.

Any time I read big miller, I get a big kick out of it. Unfortunately, it is usually very useless since it is WAY to much information - but way interesting none the less.

 

[pgg]

A period in the continuum (that doesn't always present itself), characterized by a recovery of excitatory neurons that have not been blunted by other pharmacological means but inadequate recovery of inhibitory neurons.

When you have a "smooth emergence", does the patient go through stage 2?

Patients go through stage 2 in the other direction, too.

So when you do mask inductions in kids, before you have an IV, before you've titrated in the narcotics for your "smooth emergence", what do you call that period of hyper-excitability after the kid is asleep but before it's prudent to start jabbing IV needles into them? (Usually right when the periop RN starts getting grabby.)

 

[Ignatius J]

Patients go through stage 2 in the other direction, too.

So when you do mask inductions in kids, before you have an IV, before you've titrated in the narcotics for your "smooth emergence", what do you call that period of hyper-excitability after the kid is asleep but before it's prudent to start jabbing IV needles into them? (Usually right when the periop RN starts getting grabby.)

Again, my opinion- As above, a period of hyperexcitability secondary to inhibitory neurons being blocked and excitatory neurons not being blocked. I'm not arguing against a period of hyper excitability.

Honest question for you- if a patient bucks at surgical incision, becomes tachycardia, and breath holds despite being perfectly still prior to incision, are they in stage 2? If so, why weren't they before incision when they were still? If not, why are they bucking and breath holding if they aren't in stage 2?