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Suggamadex in renal failure patients

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dchz

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This has been brought up before. I have personally gave it in > 5 renal failure patients and many many more CKD >3 pts.

All that matters is that the rate of dissociation from sugammadex molecule is slower than the rate of elimination from the liver (which it always is given the clearance of rocuronium is around .16L/kg/hr, 70% of that is liver, source)

It's safe unless your pt is end stage liver too, then it'd give it some cautions. Cyclodextrans are an inert molecule. If i recall the literature correctly, it's removed by hemodialysis.
 
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Morzh

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I've given it plenty of times to renal failure patients and never had an issue with the hypothetical re-curarization. As DCHZ explained, only a small fraction of the aminosteroid NMBs are renally eliminated - it's mostly liver / bile. While this does cause a somewhat prolonged duration of action, it does not impact the effectiveness of sugammadex.

On two occasions I've given sugammadex in PACU to patients who were given roc + neo/glyco in the OR (not by me) and 30 minutes later were in respiratory distress from residual paralysis. So in my book, in 2020 and going forwards, there are two equally safe options for ESRD patients - cisatracurium or roc+suga - and both are superior to roc+neo.

This is a case report I fond on the front page of google, and this summary paragraph puts it all together nicely:

As noted above, concern has been expressed regarding the administration of sugammadex to patients with renal failure, given the potential for prolonged excretion of the sugammadex-rocuronium complex.9 The delayed excretion has led to the theoretical concern of the dissociation of rocuronium from the sugammadex-rocuronium complex with recurrence of neuromuscular blockade. However, dissociation is minimal, as it has been estimated4,6,22 that for every 25 million sugammadex-rocuronium complexes that are formed, only one complex dissociates. No change in renal function or alteration in renal biomarkers has been noted following its use in patients with renal dysfunction.23 Additional data from the literature2325 also support safety and efficacy of sugammadex in patients with altered renal function (Table).

1594242341751.png
 
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CD125

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A couple years ago I gave a 2 mg/kg to a ESRD patient who had 2/4 twitches (relaxed with vec), she got her twitches and strength back and extubated seemingly without issue and following commands. I get called to the PACU about 30 minutes later about some hypoxia and patient was definitely floppy - gave another 2 mg/kg dose at that point which again perked her back up quickly with no further issues. Since this incident I try to avoid suggamadex in ESRD patients but if I do end up using it I go with the bigger dose just to be safe.
 
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SnapperRocks

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I've given it plenty of times to renal failure patients and never had an issue with the hypothetical re-curarization. As DCHZ explained, only a small fraction of the aminosteroid NMBs are renally eliminated - it's mostly liver / bile. While this does cause a somewhat prolonged duration of action, it does not impact the effectiveness of sugammadex.

On two occasions I've given sugammadex in PACU to patients who were given roc + neo/glyco in the OR (not by me) and 30 minutes later were in respiratory distress from residual paralysis. So in my book, in 2020 and going forwards, there are two equally safe options for ESRD patients - cisatracurium or roc+suga - and both are superior to roc+neo.

This is a case report I fond on the front page of google, and this summary paragraph puts it all together nicely:



View attachment 312246

Anyone have any thoughts on residual neostigmine induced weakness after sugammadex use as rescue?

 
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cchoukal

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It’s true that there are case series of patients having recurarization after sugammadex, and that many of those patients had renal failure, but that’s not the same as saying most patients with renal failure will have recurarization. There’s actually a pretty good module on this in the ASA education /MOCA patient safety section on their website. It is good for a few MOCA safety credits.
They cover the pros and cons of roc/sug vs cis/neo-glyco, which is also not great in patients with renal failure. I was a late convert to sug, but am a believer. The Cochrane group declared sug safer than neo-Glyco, and I bet you can dig through the 50 supplementary appendices and find a break down by renal function.
 
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MirrorTodd

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A couple years ago I gave a 2 mg/kg to a ESRD patient who had 2/4 twitches (relaxed with vec), she got her twitches and strength back and extubated seemingly without issue and following commands. I get called to the PACU about 30 minutes later about some hypoxia and patient was definitely floppy - gave another 2 mg/kg dose at that point which again perked her back up quickly with no further issues. Since this incident I try to avoid suggamadex in ESRD patients but if I do end up using it I go with the bigger dose just to be safe.
Isn't sugammadex less effective with vec vs roc? I'd imagine the recurarization was due to the reduced binding with vec and not the renal failure.
 
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2Fast2Des

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Isn't sugammadex less effective with vec vs roc? I'd imagine the recurarization was due to the reduced binding with vec and not the renal failure.

Yeah exactly my thought as well, I thought vec isn't as reliably reversed with sugammadex. Roc and sugga are the best combo
 
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CD125

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Isn't sugammadex less effective with vec vs roc? I'd imagine the recurarization was due to the reduced binding with vec and not the renal failure.

Its true its less effective but I was under the impression sugammadex works so well that its affinity for vec is still very strong. The dosing info for Bridion states that the 2 and 4 mg/kg doses are for both vec and roc while the 16 mg/kg is for roc.
 
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axeon123

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Do you guys notice more secretions on extubation with sugammadex versus neo/glyc?

And, do you guys give the entire 200mg in the vial or you dose to necessary dose based on twitches? Some people I work with with four twitches at the end decide to give the whole vile dose just because it won't be reused. When I say 200mg, meaning a 60kg patient who would have needed maybe 60-120mg based on dosing.
 
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SnapperRocks

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Do you guys notice more secretions on extubation with sugammadex versus neo/glyc?

And, do you guys give the entire 200mg in the vial or you dose to necessary dose based on twitches? Some people I work with with four twitches at the end decide to give the whole vile dose just because it won't be reused. When I say 200mg, meaning a 60kg patient who would have needed maybe 60-120mg based on dosing.

Depends on the patient and twitches. I haven’t seen more secretions but definitely less obstruction extubating deep.
 
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dchz

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Do you guys notice more secretions on extubation with sugammadex versus neo/glyc?

And, do you guys give the entire 200mg in the vial or you dose to necessary dose based on twitches? Some people I work with with four twitches at the end decide to give the whole vile dose just because it won't be reused. When I say 200mg, meaning a 60kg patient who would have needed maybe 60-120mg based on dosing.

Regularly give the whole vial. Innert molecule, very little downside. It also gives you a margin of safety against reparalyzation.
 
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SnapperRocks

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Regularly give the whole vial. Innert molecule, very little downside. It also gives you a margin of safety against reparalyzation.

Not wrong and i do sometimes too. But for example, our ICU still doesn’t appear to know what sugammadex is. Every time i drop off a sick patient that i feel like they would leave intubated if i brought them back so opt to give them a shot at extubation, i sign out that roc may not work if you have to reintubate in the next few hours. Clueless expression on their face every time.

So tend to start with textbook dose and adjust with the rest if it appears clinically necessary.
 
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woopedazz

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Regularly give the whole vial. Innert molecule, very little downside. It also gives you a margin of safety against reparalyzation.
I do too. An argument can be made that it has a relatively decent risk of Non-IgE mediated allergic anaphylaxis/non-allergic anaphylaxis so reducing dose reduces the chance of this. It's a stretch, but I can see someone doing it.
 
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jwk

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I try to have 4/4 twitches at the end of the case. I personally do not like reversing on 0-2/4 twitches. I supervise so now I just show up and cross my fingers
That's the joy of sugammadex. Megadose if no twitches, 2-4 mg/kg works on just about everyone else. In the same way that many just give 200 of sugammadex to everyone, many start with a full 50mg vial of roc, even for a shorter case, since sugammadex works so well.
 
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Brick Majors

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Regularly give the whole vial. Innert molecule, very little downside. It also gives you a margin of safety against reparalyzation.

Respectfully disagree. Have personally witnessed anaphylactic reaction to sugammadex. I would treat it like any other medication, dose it as needed, titrate to effect, use what you need to get reversal. Sugammadex is pretty convenient, and overall much safer and more effective than neo/glyco, but still has risks. I see a lot of people just pushing a vial without assessing twitches. I discourage this as a regular practice.
 
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MoMoGesiologist

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Respectfully disagree. Have personally witnessed anaphylactic reaction to sugammadex. I would treat it like any other medication, dose it as needed, titrate to effect, use what you need to get reversal. Sugammadex is pretty convenient, and overall much safer and more effective than neo/glyco, but still has risks. I see a lot of people just pushing a vial without assessing twitches. I discourage this as a regular practice.
Definitely agree we should assess twitches before dosing. I see this as done as well and it irks me to no end. How hard is it to check twitches? What if pt has zero post tetanic and we are willy nilly reversing? Sloppy. Truly sloppy
 
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dchz

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Respectfully disagree. Have personally witnessed anaphylactic reaction to sugammadex. I would treat it like any other medication, dose it as needed, titrate to effect, use what you need to get reversal. Sugammadex is pretty convenient, and overall much safer and more effective than neo/glyco, but still has risks. I see a lot of people just pushing a vial without assessing twitches. I discourage this as a regular practice.

I see your point of view.

For the sake of argument how do you know:

-it as an anaphylactic reaction?
-it was the sugamadex that caused the anaphylactic reaction?
-reducing the dose of the drug would have prevented the reaction?

I try to have 4/4 twitches at the end of the case. I personally do not like reversing on 0-2/4 twitches. I supervise so now I just show up and cross my fingers
So if you have 1 /4 twitch you don't like reversing?

Definitely agree we should assess twitches before dosing. I see this as done as well and it irks me to no end. How hard is it to check twitches? What if pt has zero post tetanic and we are willy nilly reversing? Sloppy. Truly sloppy

Are you saying if the pt has 0 post tetanic twitches then the patient has no molecule in the cleft?
 
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anbuitachi

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I try to have 4/4 twitches at the end of the case. I personally do not like reversing on 0-2/4 twitches. I supervise so now I just show up and cross my fingers

isnt that what suggamadex is for.... usually if patient has 2 twitch or less, i use sugg. more than that i use glyc/neo usually cause we have limited supply of sugg
 
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anbuitachi

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Not wrong and i do sometimes too. But for example, our ICU still doesn’t appear to know what sugammadex is. Every time i drop off a sick patient that i feel like they would leave intubated if i brought them back so opt to give them a shot at extubation, i sign out that roc may not work if you have to reintubate in the next few hours. Clueless expression on their face every time.

So tend to start with textbook dose and adjust with the rest if it appears clinically necessary.

how long does sugg last in body in normal renal function? i dont recall anymore
 
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Sugammadex (0.1-8.0 mg/kg) has a clearance rate of 88 ml/min, elimination half-life of 1.8 h, and distribution volume of 11 to 14 L [8,9]. Approximately 75% of the dose is eliminated renally; 59-80% of the dose is excreted renally in the first 24 h after administration [8].

After encapsulation by sugammadex, rocuronium is confined to the space in which sugammadex resides, and urinary excretion is the main route of elimination of the sugammadex-rocuronium complex. Administration of sugammadex diverts the elimination of rocuronium from its normal primary pathway of hepatic clearance to renal clearance [8].

When reparalysis is required, it is encouraging that sugammadex can reverse neuromuscular blockade after the reuse of rocuronium
owever, the onset time and duration of action of the second dose of rocuronium are unpredictable due to several: the dose of rocuronium, the previous dose of sugammadex, and the duration of time between drug injections, among others. It is recommended that re-injection of rocuronium (0.6 mg) should be performed 6 h after previous sugammadex administration, which is three folds of the elimination half-life of the sugammadex [18].

However, the effects of reinjected rocuronium depend on the plasma concentration of circulating free rocuronium. Thus, it is possible to induce a complete neuromuscular block by increasing the second rocuronium dose even immediately after sugammadex administration. Cammu et al. [18] reported that complete neuromuscular blockade can be induced by reinjection of 1.2 mg/kg of rocuronium 5 min after injecting 4.0 mg/kg of sugammadex.

 
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MoMoGesiologist

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I see your point of view.

For the sake of argument how do you know:

-it as an anaphylactic reaction?
-it was the sugamadex that caused the anaphylactic reaction?
-reducing the dose of the drug would have prevented the reaction?


So if you have 1 /4 twitch you don't like reversing?



Are you saying if the pt has 0 post tetanic twitches then the patient has no molecule in the cleft?
If I’m doing my own case, I titrate paralytic so I have twitches back at the end. Try not to end up in a situation where it’s only 0-1 twitches. Doesn’t always happen but that’s the goal.
 
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anbuitachi

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If I’m doing my own case, I titrate paralytic so I have twitches back at the end. Try not to end up in a situation where it’s only 0-1 twitches. Doesn’t always happen but that’s the goal.

easily done with good surgeons. then you have those surgeons who demand 0 twitch for closure...
 
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woopedazz

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I see your point of view.

For the sake of argument how do you know:

-it as an anaphylactic reaction?
Anaphylaxis is a clinical syndrome; normally pretty unlikely to be anything else if it looks like anaphylaxis and comes on within 60sec of injection. Treatment is the same regardless - assuming hypotension...

-it was the sugamadex that caused the anaphylactic reaction?
One of the top four allergens in the OT. Incidence is greater than Abx, sux, roc, chlorhex, etc. It's not quite as bad as patent blue or fish sperm.
-reducing the dose of the drug would have prevented the reaction?
Sugammadex is a notorious offender for non-IgE mediated anaphylaxis, which are classically dose dependent reactions.
 
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Urzuz

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Regularly give the whole vial. Innert molecule, very little downside. It also gives you a margin of safety against reparalyzation.

Can you define what you mean by inert in this context?

I feel like dosing a medication based on the vial it comes in is silly. Any medication should be given in the lowest dose to achieve the desired effect. Even a "medication" like normal saline has far reaching consequences if a patient gets too much of it -- why wouldn't you believe the same for sugammadex? If you have a reason to think that they may have a recrudescence of their neuromuscular blockade, fine, give a larger dose. But just because you haven't observed any downside to giving 200 mg to every patient you come across, doesn't mean that potential downsides don't exist.

There was a recent post that talked about how you should read the package insert before giving any medication. So, have you read the package insert to sugammadex? I recommend you do. Anaphylaxis, as someone mentioned, can occur. But what about coagulopathy? Bradycardia? Cardiac arrest? Again, all known side effects. The package insert also tells you how you should dose the medication.

The fact that some people think they understand the pharmacology and interactions of the drug better than the manufacturer (who, by the way, would love to tell you to give a mega dose of their medication to everyone since it just means more $$$ for them) is the height of hubris.
 
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coffeebythelake

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Can you define what you mean by inert in this context?

I feel like dosing a medication based on the vial it comes in is silly. Any medication should be given in the lowest dose to achieve the desired effect. Even a "medication" like normal saline has far reaching consequences if a patient gets too much of it -- why wouldn't you believe the same for sugammadex? If you have a reason to think that they may have a recrudescence of their neuromuscular blockade, fine, give a larger dose. But just because you haven't observed any downside to giving 200 mg to every patient you come across, doesn't mean that potential downsides don't exist.

There was a recent post that talked about how you should read the package insert before giving any medication. So, have you read the package insert to sugammadex? I recommend you do. Anaphylaxis, as someone mentioned, can occur. But what about coagulopathy? Bradycardia? Cardiac arrest? Again, all known side effects. The package insert also tells you how you should dose the medication.

The fact that some people think they understand the pharmacology and interactions of the drug better than the manufacturer (who, by the way, would love to tell you to give a mega dose of their medication to everyone since it just means more $$$ for them) is the height of hubris.

It is definitely not an inert drug. Agree that sugammadex should be dosed appropriately based on TOF/accelerometer monitoring.

Yes I've seen rapid, profound bradycardia from sugammadex
 
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MoMoGesiologist

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It is definitely not an inert drug. Agree that sugammadex should be dosed appropriately based on TOF/accelerometer monitoring.

Yes I've seen rapid, profound bradycardia from sugammadex
was that because it was overdosed or not related to dosing? How long did it last and how did you treat?
 
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coffeebythelake

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was that because it was overdosed or not related to dosing? How long did it last and how did you treat?

4 mg/kg dose sugammadex

Treated with ephedrine and atropine

HR went down to 20s within 30 seconds of giving sugammadex. NIBP couldn't read. Pulse was weak.
 
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dchz

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Sugammadex is a notorious offender for non-IgE mediated anaphylaxis, which are classically dose dependent reactions.

I would agree with your assessment if what you claim is correct.

So I guess all that's left is to convince me there is good scientific evidence that what is quoted is true.

Show me the evidence, I will concede to your assertions.
 
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anbuitachi

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4 mg/kg dose sugammadex

Treated with ephedrine and atropine

HR went down to 20s within 30 seconds of giving sugammadex. NIBP couldn't read. Pulse was weak.

Did you bolus that stuff?

I always do very slow bolus of sugammadex to decrease risk of profound bradycardia. hard to tell if it makes a difference because its rare
 
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Urzuz

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I would agree with your assessment if what you claim is correct.

So I guess all that's left is to convince me there is good scientific evidence that what is quoted is true.

Show me the evidence, I will concede to your assertions.

This is what I’m confused about. There is the potential for dose-related complications (anaphylaxis, bradycardia, etc), while giving a larger-than-required dose offers little to no benefit. Isn’t that enough reason to err on the side of caution and give a calculated dose? What is the resistance to checking twitches and doing some basic arithmetic?
 
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dchz

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Can you define what you mean by inert in this context?

The sugammadex molecule does not produce any metabolites. Source, Under metabolism and elimination.
Definition of inert: An inert chemical is one that is stable and unreactive under specified conditions.

The molecule itself is a chelator, it does not react with enzymes in the body to form metabolites, (like morphine).

I feel like dosing a medication based on the vial it comes in is silly. Any medication should be given in the lowest dose to achieve the desired effect. Even a "medication" like normal saline has far reaching consequences if a patient gets too much of it -- why wouldn't you believe the same for sugammadex? If you have a reason to think that they may have a recrudescence of their neuromuscular blockade, fine, give a larger dose. But just because you haven't observed any downside to giving 200 mg to every patient you come across, doesn't mean that potential downsides don't exist.

First, good use of the word recrudescence, props. Second, I hope the use of "you" in this paragraph is in the general sense, such as in a rant, and is not meant to address me directly. Because i have clearly shown in my posts in this thread that i have weighted the risk and benefits of giving the whole vial. I also did not assert the downside does not exist : " very little downside" - another indication of me weighing the risk and benefits.

There was a recent post that talked about how you should read the package insert before giving any medication. So, have you read the package insert to sugammadex? I recommend you do. Anaphylaxis, as someone mentioned, can occur. But what about coagulopathy? Bradycardia? Cardiac arrest? Again, all known side effects. The package insert also tells you how you should dose the medication.

I have read the insert, before I used it as a Ca-1, after having a discussion with an attending about using it on a renal failure patient and pediatric population a year later. And again today just to make sure i'm not talking out of my ass.

The fact that some people think they understand the pharmacology and interactions of the drug better than the manufacturer (who, by the way, would love to tell you to give a mega dose of their medication to everyone since it just means more $$$ for them) is the height of hubris.

Who claimed to know the pharmacology and drug interactions better than the manufacturer? Asking someone a question, not waiting for them to respond, misquoting someone's claims, then making exaggerated assertions based on those misquoted claims - that is the height of hubris.


This is what I’m confused about. There is the potential for dose-related complications (anaphylaxis, bradycardia, etc), while giving a larger-than-required dose offers little to no benefit. Isn’t that enough reason to err on the side of caution and give a calculated dose? What is the resistance to checking twitches and doing some basic arithmetic?

You are confused. I agree. You are confused because you are minimizing the benefit and exaggerating the risk to reduce my view point to absurdity.



In case you are here for a real discussion and not just randomly misquoting people:

Discussion purpose: weighing the risk and benefit of larger than recommended dose of sugammadex.

For relatablility, let's assume a fake pt of 75kg male. 2mg/kg would be 150mg (1.5cc) of sugammadex. 200mg (2.0cc) would be 2.67mg/kg.

Benefit is clear: you give more molecules to have a "sink" for the aminosteroid paralytics. Rocuronium affinity to sugammadex is well established, but what if you gave your patient vecuronium instead? What if i stimulated a muscle on one of the twitches and the pt had 1 twitch instead of 2? surely having 2.67mg/kg of sugammadex instead of 2.0 mg/kg of sugammadex (all other things equal) lessen the chance of residual blockade?

Risk is less clear:
Total list of risks: anaphylaxis, legal risk from being sued for chelating birth controls, chelating a SERM-Toremifene, treatment for breast cancer. Finally, these ominous "bradycardic" episodes.

In weighing the risk and benefit, one of the things that can elucidate the risk more clearly is more clarity on these bradycardic events which everyone is fixated on. In my attempt at understanding these episodes I have sought out the literature (this was 2 years ago, i have not been updated, so please correct me if i'm wrong). From what i saw, these events are so rare that only case reports exist. Unfortunately, none of these case reports have a unifying theme or trigger and all of them have poorly describe events around the occurrence. In fact, I had an attending that had one of these episodes, but all he was able to tell me is that there was a lot of other things going on at the same time and the pt's HR went down to 50 for 20 seconds then recovered without intervention, sugammadex was one of the drugs given.



So there you have it, the evidence on applying the risk and benefit is very hard to compare with the scarcity of literature. So in the event of incomplete information, I made my practice decision by observing the events occurring around me in my institution - ready to change my practice if i see new evidence:

In my institution, we had 30+ ORs, with approx 80-100 GETA cases daily. Majority of them used sugammadex, there was 1 event of a bradycardic episode in the last 4 years (described above). There was about 6-10 reintubations in the PACU during the same period (however, it's unclear to me how many of these are due to paralysis rather than other reasons).

In our fake pt, how consistently could I give 1.5ccs instead of 2ccs? at the beginning, i have to admit i was meticulous about giving the exact 1.3ccs of sugammadex. But this time period is also one of the most involved periods of anesthesia - the surgery is finishing, people are moving, i'm decreasing the volatile and etc. Then, what happens if the pt doesn't spontaneously breathe??? that's right, the first thing I did was give the rest of the 0.7cc of sugammadex.... I thought i saw two twitches but instead what if the 2nd twitch was just a direct stimulation of the muscle and the pt only had 1 twitch? then i'm suppose to give slightly more than 2mg/kg, right?? gradually, I started to err on the side a slight higher dose, 1.5ccs for a 60kg man instead of 1.2ccs while keeping in the back of my mind i might have slightly increased the pt's risk.

Another thing to consider: in giving the slight higher dose I can observe the immediate risk of bradycardia. I will be observing and ready to act immediately. However, that is not true for the reparalyzation scenario. It will occur in the PACU which is less controlled than the OR.

Furthermore, where did this number of 2mg/kg come from? let's be honest, the manufacture probably rounded this number to say the least. What if the optimal number is 1.7mg/kg? clearly if they are willing to round the numbers that probably tells me differences of .5mg/kg is not really significant. (this is purly conjecture. no evidence for this whatsoever).


So the reason i slightly dose higher in sugammadex is that I observe more way reintubations than bradycardic episodes in practice. I also feel like erring on the side of having more reversal shifts the pt's risk profile very favorably. However, if @woopedazz can show me that 2.0mg/kg of sugammadex will increase the anaphylactoid reactions way more than 1.5mg/kg. Then I would respond to this evidence appropriately and regress back to the described dosing on the insert.
 
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Urzuz

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The sugammadex molecule does not produce any metabolites. Source, Under metabolism and elimination.
Definition of inert: An inert chemical is one that is stable and unreactive under specified conditions.

The molecule itself is a chelator, it does not react with enzymes in the body to form metabolites, (like morphine).

Got it. I was confused because it being chemically inert has no relevance on whether or not giving too much can have physiologic effects, and it says nothing about its safety profile. There are plenty of substances that do not undergo metabolism that have physiologic impacts in our body. Just look at the inert gases...just because its inert doesn't mean you can huff radon at will without it having any impact.

Who claimed to know the pharmacology and drug interactions better than the manufacturer? Asking someone a question, not waiting for them to respond, misquoting someone's claims, then making exaggerated assertions based on those misquoted claims - that is the height of hubris.

I didn't mean for it to come off as me making assumptions about what you said, so sorry if it did.


Discussion purpose: weighing the risk and benefit of larger than recommended dose of sugammadex.

For relatablility, let's assume a fake pt of 75kg male. 2mg/kg would be 150mg (1.5cc) of sugammadex. 200mg (2.0cc) would be 2.67mg/kg.

Benefit is clear: you give more molecules to have a "sink" for the aminosteroid paralytics. Rocuronium affinity to sugammadex is well established, but what if you gave your patient vecuronium instead? What if i stimulated a muscle on one of the twitches and the pt had 1 twitch instead of 2? surely having 2.67mg/kg of sugammadex instead of 2.0 mg/kg of sugammadex (all other things equal) lessen the chance of residual blockade?

Risk is less clear:
Total list of risks: anaphylaxis, legal risk from being sued for chelating birth controls, chelating a SERM-Toremifene, treatment for breast cancer. Finally, these ominous "bradycardic" episodes.

So let me preface this by saying that I don't know if you are someone who gives 200 mg to everyone regardless of weight/depth of paralysis since you didn't explicitly say that. I know people that do, and that is the main practice that I have an issue with. If you adjust based on a patient's depth of paralysis or their weight, great. But again, many of our colleagues don't.

In your example, you pose the hypothetical that IF the patient had 1 twitch instead of 2, then yes, >2 mg/kg would be advisable. The point I am making is that you have a way to see how many twitches the patient has. If the patient has 2, give 2 mg/kg. If they have only 1, then increase the dose. If the patient has 0, 200 mg may not be enough and you may need to give more. I'm not sure if you are someone who doesn't routinely check twitches before dosing sugammadex (I personally know several), but if you are, you are blindly giving a dose without having any idea where your starting point is. Additionally, in your example, you used a 75 kg male. What if the patient is a 45 kg lady? Suddenly you're at 4.4 mg/kg and the amount of free molecule floating around has suddenly increased dramatically.

The risk is definitely NOT less clear. I don't understand why you are downplaying and even leaving out some of the potential complications associated with it. Here is a paper that was published in the past year that goes over the risks in a little more detail than you presented, and lists several other risks. I recommend you give it a read: The potential risks of sugammadex

I'll highlight a couple of lines for you: "The potential risks presented above are dose-dependent and more frequent with the free-form of sugammadex. Therefore, it is better to avoid using more than the optimal dose of the drug...Therefore, the anesthesiologists should pay more attention to prevent overdose of sugammadex...anesthesiologists need to be cautious about the potential risks until further evidence is accumulated."


In my institution, we had 30+ ORs, with approx 80-100 GETA cases daily. Majority of them used sugammadex, there was 1 event of a bradycardic episode in the last 4 years (described above). There was about 6-10 reintubations in the PACU during the same period (however, it's unclear to me how many of these are due to paralysis rather than other reasons).

I would caution you to not alter your anesthesia practice based on the ****ty practice of others. As you said, you have no idea how many of these patients were being reintubated for any number of other reasons. And those that were being reintubated for residual neuromuscular blockade, how many were dosed appropriately with sugammadex? Without actually knowing that information, these numbers are meaningless.

Another thing to consider: in giving the slight higher dose I can observe the immediate risk of bradycardia. I will be observing and ready to act immediately. However, that is not true for the reparalyzation scenario. It will occur in the PACU which is less controlled than the OR.

Again, until we have evidence to show that patients are getting reparalyzed despite sugammadex being dosed appropriately in the appropriate patient (e.g.: given rocuronium, not ESRD, etc), I am going to trust the clinical trials that the manufacturer did that enrolled thousands of patients vs anecdotal evidence that others have.

Furthermore, where did this number of 2mg/kg come from? let's be honest, the manufacture probably rounded this number to say the least. What if the optimal number is 1.7mg/kg? clearly if they are willing to round the numbers that probably tells me differences of .5mg/kg is not really significant. (this is purly conjecture. no evidence for this whatsoever).

They do dose escalation and de-escalation studies to find the optimal dose. Maybe they did round up? But as you said, it is all conjecture and neither of us know the answer to that question.

Elijah McLain and I agree. That said, I’ve never given 2340mg of Ancef or 3mg of Zofran.

Too soon :eek:

But joking aside, the reason you haven't given 3 mg of Zofran is because the 4 mg dose is what was studied by the manufacturer and it is what is recommended by the manufacturer. https://www.novartis.us/sites/www.novartis.us/files/zofran_inj.pdf

Overall I just feel like checking twitches takes all of 5 seconds, and dose adjusting takes another 5 seconds. All in all, you have spent 10 seconds to mitigate any potential complication from overdosing a drug that we are still learning about.
 
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MoMoGesiologist

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Just to preface, I agree with you 100%. This is true in the ideal world, but sometimes you don't have access to the arms or even the face (BIS + cerebral ox), or batteries are low on the twitch monitors, or they straight up don't work even after the second or third time you've called for another one from anesthesia techs who don't want to do their jobs. When the drapes come down and you're trying to keep the room moving, it becomes a lot more difficult. I'm speaking as somebody will check twitches on every single patient if logistically possible and give twitch-/weight-based dosing of reversal every time, even in the cardiac ORs.
In that case, i like to make sure they can trigger on PSV and paralytic hasn’t been given recently. Then give 4/kg. Otherwise wait til drapes are down.
 
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