Quantitative TOF monitoring

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caligas

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Just got around to reading the new ASA Guidelines, that STRONGLY recommend use of quantitative TOF monitors.

We don’t even have these monitors in our ORs and with standard TOF twitch monitors and sugamadex we have essentially eliminated PACU issues directly attributable to residual motor weakness.

Why is the ASA arming lawyers with this stuff?

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Members don't see this ad :)

For the money:

Administering sugammadex to all patients is another approach to reduce residual blockade. Sugammadex without neuromuscular monitoring appears to reduce, but not eliminate, residual blockade.21,22 Some advocate this single-drug approach because anesthesiologists do not routinely use neuromuscular monitoring.2,20,23,24 Sugammadex was introduced in Japan in 2010, and by 2014 was used for reversal in 95% of cases. Subsequently, concerns were raised about anaphylaxis25 and residual blockade.21,26 In January 2019, the Japanese Society of Anesthesiologists (Kobe, Japan) warned of the dangers of using sugammadex27 without neuromuscular monitoring...

so, yes, a solution looking for a problem....who doesn't check twitches?
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Just got around to reading the new ASA Guidelines, that STRONGLY recommend use of quantitative TOF monitors.

We don’t even have these monitors in our ORs and with standard TOF twitch monitors and sugamadex we have essentially eliminated PACU issues directly attributable to residual motor weakness.

Why is the ASA arming lawyers with this stuff?
Occam's Razor: because the people who write this garbage don't actually practice anesthesia


I favor the theory of ignorance over malice/corruption.
 
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We use neostigmine for the majority of our reversals; sugammadex is considered an avoidable expense (it pays for itself, but bean counters don't understand that).

We all know about undetectable fade where residual paralysis is still present (when using qualitative). Therefore, having quantitative monitoring available and recommending it's use is entirely appropriate.

Not sure how you can argue that quantitative monitoring is being pushed by sugammadex. Qualitative/none would make more sense. But we do get the quantitative modules getting hard selled to us at work...
 
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Has anyone actually seen inadequate reversal with sugammadex? I can’t imagine it being possible outside of some insanely boneheaded scenario where someone gets like 400 mg of roc and only 1 vial of sug.
 
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The reason for quant TOF is to be able to determine when you don’t have to reverse (or to show just how ineffective your cholinesterase inhibitor actually is)

It actually would save hospitals money. I loved using them when we had them. Unfortunately, they are easily broken and expensive so we no longer have them.

But also since we can use suggamadex as much as we want, I don’t need a twitch monitor. The diaphragm is my twitch monitor that helps me dose suggamadex.

I suspect much of the world is still using the worthless drug neostigmine. In that case, I would think Quant monitoring is imperative. I suspect that is why the ASA is suggesting it.
 
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Has anyone actually seen inadequate reversal with sugammadex? I can’t imagine it being possible outside of some insanely boneheaded scenario where someone gets like 400 mg of roc and only 1 vial of sug.
Yes, in pediatrics. I've had it happen to me twice so far (both full term infants, one was 4 weeks and one was 3 months) but there's been a few case reports about recurarization in the peds population even after adequate reversal with sugammadex.
 
Has anyone actually seen inadequate reversal with sugammadex? I can’t imagine it being possible outside of some insanely boneheaded scenario where someone gets like 400 mg of roc and only 1 vial of sug.
I've seen it happen at least once in a young average sized adult patient at an ambulatory surgery center where I thought the >2mg/kg of 200mg would do the trick, but the guy kept saying he couldn't breathe after I extubated him (everything looked fine other than him claiming dyspnea). I gave another 200mg while still in the OR and he instantly felt better and calmed down. I didn't give him a "boneheaded" 400mg of rocuronium but obviously had given him more than necessary (don't remember more exact details). I probably didn't have a nerve stimulator available as some places here don't supply them.

To answer the original topic, quantitative TOF isn't convenient to work with even if you have it. One could argue that the pause between propofol and rocuronium required to test baseline amplitude complicates initial induction and airway management a bit and it's hard to guarantee the patient's arm doesn't move throughout the whole surgery, including positioning.

One other important thing I like to point out is that just because you aren't getting called to the PACU for breathing problems doesn't mean you're not causing harm with inadequate reversal. Residual pharyngeal muscle weakness leads to increased aspiration pneumonia in hospital populations.
 
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Yes, in pediatrics. I've had it happen to me twice so far (both full term infants, one was 4 weeks and one was 3 months) but there's been a few case reports about recurarization in the peds population even after adequate reversal with sugammadex.
Could not see this unless profound paralysis were utilized...which would beg the question in peds...why? And we're back to the twitch monitoring issue....
 
I think the weight based dosing for suggamadex is faulty. 1 mg roc is bound by 3.6mg of suggamadex so I dose accordingly.

50 of roc gets 200mg Sugg, etc, twitches don’t matter.

If I have someone I’m worried about clearance of roc and they’ve gotten more than 200 mg in a long case (our APPs love roc infusions, don’t get me started), I’m generous with it, almost always 4mg/kg minimum dose even with twitch recovery.

I prefer vec for maintaining paralysis, it has a lower receptor affinity (1mg vec to 9mg sugg) but is more potent, 20mg of vec goes much longer than 50 of roc.
 
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Could not see this unless profound paralysis were utilized...which would beg the question in peds...why? And we're back to the twitch monitoring issue....
Profound paralysis had not been utilized in either of the two cases that I did. One did get RSI dosing of roc at 1.2 mg/kg for a lap pyloro, they had TOF 0/4 on qualitative monitoring about an hour later, and was given 4 mg/kg of sugammadex but still appeared weak and floppy, gave a 2nd dose of 4 mg/kg, and was able to extubate with no issue after the 2nd dose. In the other case, patient was undergoing a nephrectomy with last dose of rocuronium 0.7 mg/kg probably about two hours before, qualitative TOF 1/4, given 4 mg/kg of sugammadex, initially looked okay in PACU but 30 min later had respiratory distress that resolved with a second dose of sugammadex.

Here's the case reports I mentioned:
Residual Weakness and Recurarization After Sugammadex Administration in Pediatric Patients: A Case Series - PubMed
Postoperative Recurarization in a Pediatric Patient After Sugammadex Reversal of Rocuronium-Induced Neuromuscular Blockade: A Case Report - PubMed
http://www.anestesiarianimazione.com/PACCJ 2020/Sugammadex and recurarization in an infant.pdf

I don't know how often you do peds anesthesia (I practice 100% peds) but quantitative TOF monitoring in this patient population, especially infants, is still tricky although becoming more feasible with some of the newer devices coming out. The recurarization after adequate NMB reversal might be related to immature receptors although that's still TBD as well.
 
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Ever since we got suggamadex, if the case lasts longer than an hour I induce with 100 of roc. Less time waiting for intubating conditions. Haven’t used a twitch monitor in years. Never had a problem. If I suspect I used a little too much roc i just give 400 suggamadex.
 
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I heard they're making fancier TOF monitors that don't require calibration for each patient like the accelerometer ones do.
But I'm not waiting around after induction to calibrate before pushing roc and I'm definitely not doing it on an awake pt.

I think it'd be neat to have in the OR, esp if the TOF slaved over to EMR so I didn't have to manually enter my TOFs. The bean counters who refuse to let us use sugammedex at some places should be forced to get us quant TOF so I feel safer reversing with neo/glyco on certain patient populations.
 
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You don't need to calibrate them.

We know that the majority of accelerometers register full NM function as 120-130% (not 100%). Therefore to get a 0.9 result you really need to just aim for 100-110% on the TOFR at the end of the case. No need to calibrate.
 
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The reason for quant TOF is to be able to determine when you don’t have to reverse (or to show just how ineffective your cholinesterase inhibitor actually is)

It actually would save hospitals money. I loved using them when we had them. Unfortunately, they are easily broken and expensive so we no longer have them.

But also since we can use suggamadex as much as we want, I don’t need a twitch monitor. The diaphragm is my twitch monitor that helps me dose suggamadex.

I suspect much of the world is still using the worthless drug neostigmine. In that case, I would think Quant monitoring is imperative. I suspect that is why the ASA is suggesting it.
The diaphragm . . . the poor man’s twitch monitor. I figure if they are reliably triggering the vent, they’ve gotta have at least 1/4 twitches and thus dose at 2mg/kg sugammadex
 
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There are people in this business who would like to make every case a major complicated drama event. They love adding unnecessary gadgets (like a quantitative TOF monitor) , using unnecessary medications, and they see zebras at every corner.
They are in every practice and everyone usually knows who they are.
They live in their own world of shiit and that's where they belong. Don't let yourself get dragged into that world of shiit.
 
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There are people in this business who would like to make every case a major complicated drama event. They love adding unnecessary gadgets (like a quantitative TOF monitor) , using unnecessary medications, and they see zebras at every corner.
They are in every practice and everyone usually knows who they are.
They live in their own world of shiit and that's where they belong. Don't let yourself get dragged into that world of shiit.
I agree but I’m thought that practice guidelines are based on survey results of practicing anesthesiologists. They are obviously not getting a random sample.
 
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I think the weight based dosing for suggamadex is faulty. 1 mg roc is bound by 3.6mg of suggamadex so I dose accordingly.

Agreed

We've argued this very point here before. It'll take time to get past the manufacturer recs though, same way we still have people running 2 L/min fresh gas flows with sevoflurane.

The only advantage of higher dosing is hastening onset of reversal. But unless you're dealing with a lost airway situation and want to restore respiratory efforts immediately that's not really an issue.
 
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I did my entire residency training on a simple TOF twitch monitor and neo/glyco. Now we have sugammadex which is basically a wonder drug for reversal of neuromuscular blockade.... and they want us to use an accelerometer? They are years behind in making this recommendation, back when it might actually make a big difference. I will PASS
 
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I agree but I’m thought that practice guidelines are based on survey results of practicing anesthesiologists. They are obviously not getting a random sample.
The cynical side of me wonders if survey response rate is tilted toward the kind of anesthesiologists you don't want doing your anesthesia. :)
 
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Agreed

We've argued this very point here before. It'll take time to get past the manufacturer recs though, same way we still have people running 2 L/min fresh gas flows with sevoflurane.

The only advantage of higher dosing is hastening onset of reversal. But unless you're dealing with a lost airway situation and want to restore respiratory efforts immediately that's not really an issue.

Drives me nuts when I see people running 2 L+ on iso or tiva
 
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Why does it bother you for a TIVA?

Because why waste the gas? It's not like the hospital is concentrating their own oxygen, it comes in large heavy cylinders that need to be transported by truck.

I forget the exact number but the amount of emissions makes inhalation anesthesia better environmentally if you use too much oxygen. I think it was around 4 L/min. I try to minimize my oxygen use, hate it when I see people giving 10L/min by mask for someone who doesn't need it. It is even worse when people disconnect the patient and leave the oxygen going after they leave the room or even all night/weekend.
 
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Emission wise, running TIVA + flows of 5-6L/min is the best for the environment. Higher flow rate offsets the CO2 absorber getting done too early, which is a big energy cost.
 
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Emission wise, running TIVA + flows of 5-6L/min is the best for the environment. Higher flow rate offsets the CO2 absorber getting done too early, which is a big energy cost.

Higher flow rate offsets the CO2 absorber getting done too early?
Please explain. Because that's not how I understand it.
 
As FGF decreases --> more rebreathing/less scavenging --> more CO2 needing to be absorbed --> rapid depletion of absorber.

Higher flow rate offsets the CO2 absorber getting done too early?
Please explain. Because that's not how I understand it.
Also... Here's a paper on the cost benefit. I thought there was another floating around on the environmental aspect... I'm on nights and will try to find it.
 

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Higher flow rate offsets the CO2 absorber getting done too early?
Please explain. Because that's not how I understand it.
The chief downside to low fresh gas flow / closed circuit anesthesia is consumption of the CO2 absorbent.

Higher flows mean some exhaled CO2 exits the circuit via the scavenger into the vacuum system, instead of being sequestered in the CO2 absorbent.


Edit to add a diagram - the important bit is that the scavenger (APL pop off in manual mode) removes excess volume before rebreathed gas goes through the absorbent.

2quKLvxy5it6oYySN98new_b.png


Back in the days before the anti global warming movement took desflurane away from us, I'd do a day of low flow des general anesthetics at about 0.5 lpm and it'd completely consume at least one cannister of absorbent.
 
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As FGF decreases --> more rebreathing/less scavenging --> more CO2 needing to be absorbed --> rapid depletion of absorber.


Also... Here's a paper on the cost benefit. I thought there was another floating around on the environmental aspect... I'm on nights and will try to find it.

ok i get the first part.
we up the FGF when the CO2 absorber is near end-of-life to (briefly) drive down the FiCO2 by the same idea.
but.. what about high FGF causing dessication of the absorber reducing the product lifespan?
even in those without the strong bases (and the dangers inherent)?

as a related question, how efficient are our HMEs in retaining heat and moisture at high FGF rates >6lpm?

Edit: seems like some of these are addressed in the discussion section
 
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The chief downside to low fresh gas flow / closed circuit anesthesia is consumption of the CO2 absorbent.

Higher flows mean some exhaled CO2 exits the circuit via the scavenger into the vacuum system, instead of being sequestered in the CO2 absorbent.


Edit to add a diagram - the important bit is that the scavenger (APL pop off in manual mode) removes excess volume before rebreathed gas goes through the absorbent.

2quKLvxy5it6oYySN98new_b.png


Back in the days before the anti global warming movement took desflurane away from us, I'd do a day of low flow des general anesthetics at about 0.5 lpm and it'd completely consume at least one cannister of absorbent.
Good point! Never thought about that. What is the cost and environmental impact of consuming and disposing absorbent?
 
Are those co2 absorbers really that expensive cause I'm the low flow king at my shop?
Years ago at the Navy joint we bought 5 gallon buckets full of absorbent granules. When the stuff in the machine was used up, the purple granules would get thrown away and replaced by new ones. Same canister. I think that has got to be the low $ mark for moles of CO2 turned into rocks.

Somewhere along the line the new Drager machines we got there had completely disposable proprietary absorbent canisters. I don't know what those cost. $7 apiece? $17? $37? Way more, I'm sure.
 
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Years ago at the Navy joint we bought 5 gallon buckets full of absorbent granules. When the stuff in the machine was used up, the purple granules would get thrown away and replaced by new ones. Same canister. I think that has got to be the low $ mark for moles of CO2 turned into rocks.

Somewhere along the line the new Drager machines we got there had completely disposable proprietary absorbent canisters. I don't know what those cost. $7 apiece? $17? $37? Way more, I'm sure.

I trained with those
When you pour the new bucket, the sheer amount of dust gives you asthma and copd
 
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Because why waste the gas? It's not like the hospital is concentrating their own oxygen, it comes in large heavy cylinders that need to be transported by truck.

I forget the exact number but the amount of emissions makes inhalation anesthesia better environmentally if you use too much oxygen. I think it was around 4 L/min. I try to minimize my oxygen use, hate it when I see people giving 10L/min by mask for someone who doesn't need it. It is even worse when people disconnect the patient and leave the oxygen going after they leave the room or even all night/weekend.
One thing no one seems to talk about (except for in this thread) is the first and environmental impact of those disposable CO2 absorbent canisters versus cost/impact of running higher fresh gas flows. Makes the discussion less black and white.
 
As FGF decreases --> more rebreathing/less scavenging --> more CO2 needing to be absorbed --> rapid depletion of absorber.


Also... Here's a paper on the cost benefit. I thought there was another floating around on the environmental aspect... I'm on nights and will try to find it.
Thank you for sharing that paper! I have wondered about that many times!
 
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