Reverse everybody?

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Noyac said:
do you pay attention? I'm in an All MD practice.
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Do I pay attention? You're the one who just asked me if I was in the military. :laugh:


Noyac said:
But if I had crna's doing cases I wouldn't be in a room for the sake of the pts that the nurses are trying to knock off. The military seems to think that this is ok I guess.
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The military does think it's OK.

Of course, so does the entire state of California.

Actually, there's arguably less CRNA supervision and MD-backup available at your average California hospital than at that big Navy joint overlooking San Diego.

Where were you going with this again? Oh, right - arguing with me for the sake of arguing. 🙄


I'm glad you work in an all-MD practice. Hope it lasts. I give $ to ASAPAC every month, but I'm not optimistic that many practices like yours will exist 10 or 20 years from now.
 
Noyac said:
This from the mod that had no idea that he couldn't post.
Click to expand...

There's no reason for him to be unable to post. He's off post hold, not banned. Ergo, why on earth would I have any reason to think he couldn't post?


The only evidence I have that he "can't" post is
a) I don't see him posting
b) You say he says he's having trouble

It seems more likely to me that the reason he isn't posting is because he doesn't want to.

Or maybe he wore out the caps lock key on his computer and can't type in his case-sensitive password. Hell if I know.


This is the last I'll write on this subject: there is no doublesupersecret stealthban going on. Take my word for it, or not. Believe me, or not. I'm done arguing this point with you.
 
Noyac said:
seriously? Weakness, nausea, vomiting, tachycardia, ischemia are a few things that come to my mind.
If you are reversing a pt that doesn't need it, then you may be inducing weakness, No? So let me ask you something, if you don't reverse and the pt shows signs of weakness, does that mean you can't add reversal? You say potential brain death. Are you not a clinician that can tell when your pt may need assistance? Do you leave a pt in the pacu that you are not totally certain that they are safe?
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Where is your data coming from (and let's talk evidence and not anecdote or feelings). First, how about posting some evidence that the use of neostigmine, as we use it in our practice, contributes to weakness.

Nausea, vomiting while uncomfortable end points. But let's use them since they are apparently important to you. The best study I've been able to find is a systematic review of available literature (PubMed ID 10434820). They found that omitting reversal prevented early nausea (relative risk 1.04 CI 0.76-1.43), early vomiting (RR 1.03 CI 0.86-1.22, late nausea (RR 1.11 CI 0.93-1.33), late vomiting (RR 0.98 CI 0.75-1.28). All cross unity, which means the results are not statistically significant.

As for the tachycardia, ischemia concern. I know how to reverse a patient without increasing the heart rate, so I'm going to assume a seasoned pro like yourself does too.

What about the point that the use of neostigmine is associated with increased hypoxic events? From the article you posted to start the thread, the odds ratio of was 1.09, confidence interval 0.98-1.21. Again, not statistically significant (nevermind drawing conclusions from an unpublished abstract that was a retrospective review).

The concern of residual muscle weakness without reversal is real and common. 7% of patients without reversal have residual weakness and that is associated with postoperative pulmonary complications (Berg 1997). The number needed to harm is 30 for clinically relevant residual weakness without reversal.

So, Noy, show me that the use of reversal is associated with increased weakness and harm? You haven't convinced me to change my practice.
 
Noyac said:
Not gonna argue point #1 with ya.
But let me ask some of the youngsters here, why is this the case?

I will say that I have gotten away with it tho.
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Just read about this...

At high concentrations, nondepolarizing NMBDs not only antagonize the alpha subunits of the AChR, they plug channel directly. Thus, even if there is enough ACh in the synaptic cleft to out-compete the NMBD and stimulate the alpha subunits, no ions can physically pass through the channel and depolarize the membrane.

Is that what you were looking for?
 
sevoflurane said:
Elimination 1/2 life for ROC would mean the amount of drug that is physically removed from the body via hepatic/billiary/renal mechanisms. I'm more interested in distribution away from the neuromuscular junction. 5 elimination 1/2 live's of 60-80 minutes is way too conservative to use in the clinical environment IMHO. That's not mentioning the 30-40% that remains protein bound and never makes it to the neuromuscular junction in the first place. Good points to bring up though. Just my 2cents.
Click to expand...

As you can imagine, I don't agree with your conclusion. If you use distribution t1/2 instead of elimination t1/2 there will be residual plasma paralytic to cause problems. If you wait your 60 minutes, at least 50% of the rocuronium will still be present. That's too much. The difference in elimination t1/2 with changing renal function is probably the cause for the highly variable response patients have to roc.
 
Use of Reversal Drugs to Reduce Residual Paralysis







Because clinical judgment can easily err, general opinion favors administration of an

anticholinesterase inhibitor at the end of anesthesia [21]. However, many practitioners avoid the

use of reversal drugs because of their potential side effects (e.g., increased the incidence of

postoperative nausea and vomiting [PONV]). Recent, systematic reviews of the published studies

report that the incidence of PONV and the need for antiemetics does not increase with the use of

neostigmine [22, 23]. Because of the potential for detrimental effects of residual paralysis [4-6],

particularly in an outpatient setting, it is necessary that reversal drugs be used without hesitation.

Using appropriate dose of reversal drugs matched for the degree of blockade should avoid the side

effects of reversal drugs.

Once it is decided to reverse the neuromuscular blockade, it is important to determine the

appropriate dose of neostigmine; however, this

G





reach a given response is reduced if a large neostigmine dose is administered, this does not mean

that a large dose is always indicated. In fact, when spontaneous recovery is almost complete, large

doses might, at best be unnecessary. In addition, it must be noted that doses of neostigmine larger

than necessary can exacerbate the muscle paralysis [24]. Unwarranted administration of

neostigmine (i.e., administration after recovery of the TOF ratio 　-&

upper airway

collapsibility, presumably by impairing upper airway dilator muscle activity [25]. Access of

neostigmine can also lead to muscle weakness [26].


http://www.cucrash.com/Handouts10/14%20Joshi%20New%20Concepts%20in%20Neuromuscular%20Blockade.pdf






 
Anesthesiology. 2010 Dec;113(6):1280-8.
Neostigmine/glycopyrrolate administered after recovery from neuromuscular block increases upper airway collapsibility by decreasing genioglossus muscle activity in response to negative pharyngeal pressure.

Herbstreit F, Zigrahn D, Ochterbeck C, Peters J, Eikermann M.
Source

Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Essen, Germany. [email protected]

Abstract

BACKGROUND:

Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function.
METHODS:

We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges.
RESULTS:

Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection.
CONCLUSION:

Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.
 
BLADEMDA said:
Anesthesiology. 2010 Dec;113(6):1280-8.
Neostigmine/glycopyrrolate administered after recovery from neuromuscular block increases upper airway collapsibility by decreasing genioglossus muscle activity in response to negative pharyngeal pressure.

Herbstreit F, Zigrahn D, Ochterbeck C, Peters J, Eikermann M.
Source

Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Essen, Germany. [email protected]

Abstract

BACKGROUND:

Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function.
METHODS:

We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges.
RESULTS:

Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection.
CONCLUSION:

Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.
Click to expand...

This study is why I don't use more than 20 ug/kg of Neostigmine if I have a TOF and DBS. Please notice they used 30 ug/kg of Neostigmine in patients with TOF of 1.0.

Low dose reversal (10-15 ug/kg) has never been shown to cause any harm in a clinical setting. Hence, I support and practice low dose reversal on a routine basis provided TOF has recovered sufficiently (Tetany without fade).
 
BLADEMDA said:
Anesthesiology. 2010 Dec;113(6):1280-8.
Neostigmine/glycopyrrolate administered after recovery from neuromuscular block increases upper airway collapsibility by decreasing genioglossus muscle activity in response to negative pharyngeal pressure.
Click to expand...

Interesting. Next time I administer rocuronium infusion without anesthesia (the study protocol) I won't reverse.
 
Interesting topic.

Our practice varies with attending.

In general, I won't reverse until I have one twitch on a train-of-four. If I have four twitches, I will check a tetany. If I get a 5-second tetany without fade, then I won't reverse, as studies have shown that it is adequate recovery of neuromuscular function.

How many institutions out there don't monitor NM blockade? Just curious?

Very interesting paper. Thanks for posting.
 
My approach has always been:

1-2 twitches: 70mcg/kg
3-4 twitches with fade: 50 mcg/kg
4 twitches without discernible fade but dose given <1 hr ago: 30 mcg/kg
4 full twitches without dose given in last hour: nothing

I will probably start to play with 10-20 mcg/kg doses after reading the citations included in this thread. Good discussion.
 
proman said:
Interesting. Next time I administer rocuronium infusion without anesthesia (the study protocol) I won't reverse.
Click to expand...

Yes, I do understand that these were healthy, young adults with no anesthesia on board. In addition, the study was under-powered in my opinion.

Again, I'm trying to present the facts for safe, effective care of patients who have received NMB in the O.R. I couldn't leave out that study.

But, there are at least a half dozen other studies showing the benefit of reversal. Again, I'm a proponent of low dose reversal in the right setting. I use more low dose reversal than any other dosage in my practice. I used to use 20 ug/kg routinely but over the past 24 months have dropped back to 10-15 ug/kg.

Those who give FULL DOSE REVERSAL to everyone should consider the evidence presented on this thread about reducing the dosage. Those who don't reverse at all should consider the evidence about the importance of low dose reversal.
 
BLADEMDA said:
Yes, I do understand that these were healthy, young adults with no anesthesia on board. In addition, the study was under-powered in my opinion.

Again, I'm trying to present the facts for safe, effective care of patients who have received NMB in the O.R. I couldn't leave out that study.

But, there are at least a half dozen other studies showing the benefit of reversal. Again, I'm a proponent of low dose reversal in the right setting. I use more low dose reversal than any other dosage in my practice. I used to use 20 ug/kg routinely but over the past 24 months have dropped back to 10-15 ug/kg.

Those who give FULL DOSE REVERSAL to everyone should consider the evidence presented on this thread about reducing the dosage. Those who don't reverse at all should consider the evidence about the importance of low dose reversal.
Click to expand...

I can see cutting down my neostigmine dose but for the moment the risk-benefit ratio still heavily favors reversing.
 
Just a CA-1 here

I don't reverse everyone. Some attendings have more/less strong opinions about this. I base my reversal dosing from Baby Miller. I usually give neo at 50mcg/kg for 1-2 twitches. As low as 20mcg/kg for 4 with fade. I started using smaller doses for reversal after I saw another resident cause paradoxical weakness with a full reversal dose in a patient with 4 twitches and fade. Anyone else ever seen this?
 
DrBeaker said:
Just a CA-1 here

I don't reverse everyone. Some attendings have more/less strong opinions about this. I base my reversal dosing from Baby Miller. I usually give neo at 50mcg/kg for 1-2 twitches. As low as 20mcg/kg for 4 with fade. I started using smaller doses for reversal after I saw another resident cause paradoxical weakness with a full reversal dose in a patient with 4 twitches and fade. Anyone else ever seen this?
Click to expand...

Please provide peer reviewed evidence for your statements. As an Attending I would want to know about your "opinion" on this matter if you were my Resident. Again, please provide anything from a credible source that your technique is both safe and effective.

One you realize that you are are not following established recommendations here perhaps you should discuss this with your attendings.

http://anesthesiologyrounds.ca/crus/122-047%20English.pdf
 
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DrBeaker said:
Just a CA-1 here

I don't reverse everyone. Some attendings have more/less strong opinions about this. I base my reversal dosing from Baby Miller. I usually give neo at 50mcg/kg for 1-2 twitches. As low as 20mcg/kg for 4 with fade. I started using smaller doses for reversal after I saw another resident cause paradoxical weakness with a full reversal dose in a patient with 4 twitches and fade. Anyone else ever seen this?
Click to expand...


I didn't mean to sound overly harsh in my previous post. However, it is my policy that every patient receive reversal agent (low dose 10-15 ug/kg) if given a non depolarizing agent within the last 90 minutes. Since I am the attending I call the shots. I would not approve of your skipping reversal whenever it suited you.

Second, low dose reversal works just fine with a TOF but I do prefer at least 20 ug/kg if there is any fade whatsoever. I wouldn't have any major issues with your reversal dosages. Here is the landmark article referencing low dose reversal:

http://www.utswanesthesia.com/education/images/stories/Journal%20Club%20Articles/Departmental_Journal_Club/Antagonim_of_Low_Degrees_of_Atracurium-induced_Neruomuscular_Blockade.pdf

When given at a TOF ratio of either 0.4 or 0.6, time to 0.9 and

1.0 TOF ratio was significantly shorter with any dose of neostigmine

than without. The probability of successful reversal after 20 ug/kg

neostigmine was 100% when a TOF ratio of 0.9 was the target; for a

TOF ratio of 1.0, the probability was 93% and 67%, dependent on

whether the dose of neostigmine was given at TOF ratio of 0.6 or 0.4,

respectively. With a dose of 30 ug/kg, a TOF ratio of 1.0 is expected to

be reached within approximately 5 min. Low doses of neostigmine are

required to reach a TOF ratio of 0.9 or to accept an interval of 10 min.






 
Guess I was unclear in my previous post. I don't reverse everyone. But I don't forego reversal if a patient needs it, I always reverse 4 twitches with fade. And I'll low-dose reverse people who have full twitches and no fade, but it has been only somewhere between 90-120 minutes since last dose. This is where some of my attendings differ. Some have a cutoff of 90min, some 2 hrs, and others 3 hrs. Didn't mean to make it sound like I give someone an intubating dose of roc (0.6mg/kg) for a chole and not reverse them at the end of the case if they need it.

http://www.ncbi.nlm.nih.gov/pubmed?term=antagonism%20of%20low%20degrees%20of%20atracurium

This paper made me think about my reversal doses and I lowered my reversal dosing because of it. That plus I saw another resident give a patient a bigger reversal dose than needed. Patient got paradoxical weakness, floppy fish, and went to the SICU intubated until neuromuscular function was adequate for extubation.
 
And my reversal dosing from baby miller comes from chapter 12, table 12-7.

Based off this article...
http://www.ncbi.nlm.nih.gov/pubmed/1416176

I remember starting out CA-1 and some of my classmates gave full reversal to everyone. I used this chart, and haven't had a problem yet. Not sure if these are up to blade standards, but it's all I got. Curious what blade and others think about paradoxical weakness. Anyone else seen it?
 
DrBeaker said:
And my reversal dosing from baby miller comes from chapter 12, table 12-7.

Based off this article...
http://www.ncbi.nlm.nih.gov/pubmed/1416176

I remember starting out CA-1 and some of my classmates gave full reversal to everyone. I used this chart, and haven't had a problem yet. Not sure if these are up to blade standards, but it's all I got. Curious what blade and others think about paradoxical weakness. Anyone else seen it?
Click to expand...

I provided you with an updated artcle (2009) from the same author quoted in your reference.

I haven't had any issues with low dose reversal even if it has been over 2 hours since the last dose of NMB. I suspect it is because 10 ug/kg of Neostigmine doesn't cause any weakness even if the TOF is 0.9/1.0.

I don't encourage full dose reversal routinely at the end of a case (see my previous posts for a better explanation). I may have had one situation where a CRNA gave 70 ug/kg of Neostigmine to patient who had not received NMB for 2 hours. This patient was indeed weak in the PACU.
 
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