Recurarization after sugammadex?

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fakin' the funk

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Curious if anyone has seen or heard about this entity.

I recently became aware of it - case was a long open abdominal case with a large amount of rocuronium given over 8+ hours, reversed apparently adequately with sugammadex at extubation and then patient became floppy in PACU 45+ minutes later. Immediately improved with second dose of sugammadex.

There are several case reports and series out there that are roughly similar. Common thread seems to be large cumulative doses of roc. The idea of a central "depot" of roc that sugammadex can't access is scary, especially in light of the ESRD thread currently going.

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Curious if anyone has seen or heard about this entity.

I recently became aware of it - case was a long open abdominal case with a large amount of rocuronium given over 8+ hours, reversed apparently adequately with sugammadex at extubation and then patient became floppy in PACU 45+ minutes later. Immediately improved with second dose of sugammadex.

There are several case reports and series out there that are roughly similar. Common thread seems to be large cumulative doses of roc. The idea of a central "depot" of roc that sugammadex can't access is scary, especially in light of the ESRD thread currently going.

Did they check twitches? Sugammadex’s Half life is twice that of neostigmine. Wouldn’t a central depot have the same recurarization effect with neostigmine? I would bet more likely explanation is that they underdosed. I can see an argument for siding with a higher dose in cases like you describe.

I’ve certainly been in long cases where i can’t get twitches on the arm or face yet still have dosed further muscle relaxant based on vent dyssynchrony. I could see that complicating deciding on a reversal dose.

Side note: In residency, if i had to take over a case, i would always make a point to check post tetanic twitches to see if the monitor was working. Sustained tetanus then train of four usually gives you an answer even with deep paralysis.
 
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Seems suspicious for too low a dose of sugammadex. Doubt the depot theory.
 
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Curious if anyone has seen or heard about this entity.

I recently became aware of it - case was a long open abdominal case with a large amount of rocuronium given over 8+ hours, reversed apparently adequately with sugammadex at extubation and then patient became floppy in PACU 45+ minutes later. Immediately improved with second dose of sugammadex.

There are several case reports and series out there that are roughly similar. Common thread seems to be large cumulative doses of roc. The idea of a central "depot" of roc that sugammadex can't access is scary, especially in light of the ESRD thread currently going.
Thought the same as @SnapperRocks. How was the suggamadex dosed?
 
I’m also suspicious of this.

roc is mostly biliary excretion, small amount of renal excretion. Suggs maddy is still longer half life than roc. Don’t understand this central depo theory.
 
Also saw a patient of a colleague in recovery after ERCP. Obese (130kg) older (70's) guy had gotten 100mg of Roc for a 60m ERCP. Reversed with 400mg of Sugammedex. Doing well sitting up until 30 minutes into recovery. Started to behave like a fish out of water-->Bipap-->400mg additional Sugammedex and suddenly looking like a rose again.

If roc’s half life is 73min and you give 100mg, an hour later would be equivalent to giving 50mg of roc and expecting 400mg of sugammadex to fix it. Unlikely you’d have any twitches after 50mg of roc. 4mg/kg would be 520mg dose for someone with post tetanic twitches. This is again, inappropriate dosing, not a zebra compartment model.

This is also why I personally prefer succinylcholine to rocuronium with potentially quick cases like ERCPs. It’s hard to know what dose to give shortly after an RSI dose of roc if you decided to RSI.
 
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It is always difficult to speak to anecdote. In this particular case, the patient was given 400mg of Sugammadex not based on TOF or post-tetanic measures but “as the patient was coughing and reaching for the tube.” That, to me, indicates appropriate timing of reversal with Sugammadex. I obviously should have included that in the scenario.
Seems like the type of story that I wouldn’t believe unless it happened to me personally.
 
Curious if anyone has seen or heard about this entity.

I recently became aware of it - case was a long open abdominal case with a large amount of rocuronium given over 8+ hours, reversed apparently adequately with sugammadex at extubation and then patient became floppy in PACU 45+ minutes later. Immediately improved with second dose of sugammadex.

There are several case reports and series out there that are roughly similar. Common thread seems to be large cumulative doses of roc. The idea of a central "depot" of roc that sugammadex can't access is scary, especially in light of the ESRD thread currently going.

For all of you saying "the sugammadex dose must have been insufficient," in this case was 2/kg given for apparent 4/4 TOF. Technically, that's "sufficient" based on the dosing guidelines I'm aware of. In this case, no post reversal TOF/tetany was assessed - is anyone routinely doing this?

I would argue sure, easy to say "insufficient dose" for reversal but this would logically also require revision of the way we dose sugammadex for repeated/high doses of rocuronium. Eg, should the sugammadex dose also be at least 1x or 2x the total roc given?

Case series as mentioned previously
 
This is also why I personally prefer succinylcholine to rocuronium with potentially quick cases like ERCPs.
This i why i just skip mucle relaxant altogether: just spray cords and trachea with lido intubate and let them ride on SV with sevo.
 
There was an APSF newsletter a good while back that described sugammadex, and referenced literature that it binds rocuronium at 3.57 mg/mg, meaning a 200mg vial of sugammadex reverses up to ~57mg of rocuronium. Unless you need reversal to occur very rapidly, you never need to overdose this ratio as far as I can see. I always ask myself, do I think there is more than 57 mg of rocuronium still floating around his patient? I have used the medication almost exclusively as my reversal agent for over 2 years without a single PACU respiratory complication, NMB related or not. Follow the link below for that ratio information.

 
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There was an APSF newsletter a good while back that described sugammadex, and referenced literature that it binds rocuronium at 3.57 mg/mg, meaning a 200mg vial of sugammadex reverses up to ~57mg of rocuronium. Unless you need reversal to occur very rapidly, you never need to overdose this ratio as far as I can see. I always ask myself, do I think there is more than 57 mg of rocuronium still floating around his patient? I have used the medication almost exclusively as my reversal agent for over 2 years without a single PACU respiratory complication, NMB related or not. Follow the link below for that ratio information.


I respect that you're following advice from APSF but I STRONGLY disagree. The context of that ratio mentioned in the APSF article is a paragraph in a review article in Anesthesiology describing the molecule in theory, not the appropriate dosing. APSF recommended lowest possible dose due to concerns of supposed dose related likelihood of anaphylaxis. Appropriate dosing is later discussed in that same Anesthesiology article, at which point they recommend actual body weight dosing with the recommended doses we all know from the package insert. Additionally, they cite research saying even this can be inadequate, particularly when objective neuromonitoring is not performed.

-----------------------

This is the quote from the APSF article:
"With antibiotics, muscle relaxants, and latex, we expect and generally see reactions early in an OR case. Unlike these, sugammadex is typically administered at the end of a case. Thus a distinct difference is the timing of the anaphylaxis presentation and vigilance for anaphylaxis that may occur at what is historically an unexpected time for such an event. When sugammadex anaphylaxis happens, it seems to occur within 5 minutes of administration.5 Interestingly, the likelihood of anaphylaxis with sugammadex appears to be dose-related.3 Therefore, it would make sense to use the lowest effective dose to decrease the incidence of anaphylaxis. As an approximate rule of thumb, it requires 4 mg (3.57 mg to be exact) sugammadex to encapsulate/antagonize 1 mg rocuronium; thus a 200-mg reversal dose is adequate for most cases.6"

If you go source 6:

Sugammadex:

A decade ago, because of the limitations inherent in the use of acetylcholinesterase inhibitors as antagonists of neuromuscular block, it seemed clear that the issue of postoperative residual block was unlikely to disappear unless an alternative method of pharmacologic reversal of deep and even moderate block became available. In 2006, articles by de Boer et al.80,81 and others82,83 described a new and promising agent.84 Sugammadex (a modified γ-cyclodextrin) forms 1:1 complexes with aminosteroid neuromuscular blocking drug molecules but has no effect on benzylisoquinolinium compounds or on succinylcholine. A dose of 3.57 mg sugammadex is needed to encapsulate 1.0 mg rocuronium. The resulting complex has a very low dissociation rate. Encapsulated molecules of the NMBA that circulate in the plasma are no longer able to bind with muscle acetylcholine receptors, allowing blocking agents to diffuse away from the synaptic cleft and back into the plasma as the concentration of free drug in plasma decreases precipitously. Thus, clinicians now have for the first time the ability to rapidly and completely reverse profound nondepolarizing neuromuscular block, and do so directly by inactivating the activity of the NMBA, rather than indirectly, by inhibiting acetylcholinesterases.

Dosing:

These studies suggesting that residual neuromuscular block may still occur after sugammadex reversal need special mention. Because of the 1:1 molar ratio between sugammadex and the aminosteroid NMBA, there have to be sufficient sugammadex molecules administered to encapsulate all of the free molecules of the NMBA. For this reason, sugammadex reversal dose is calculated based on the depth of neuromuscular block at the time of reversal. For reversal of moderate block (TOFC, 1 to 3), a dose of 2 mg/kg is recommended; for reversal of deep block (PTC more than or equal to 1), a dose of 4 mg/kg is recommended, and for rescue from a failed rapid-sequence induction in the cannot-intubate-cannot-ventilate scenario (profound block, PTC = 0), a dose of 16 mg/kg is recommended (table 3). Therefore, if clinicians use subjective or clinical means of assessment of neuromuscular block rather than objective monitoring, it is possible that the dose of sugammadex may be insufficient, resulting in incomplete reversal. This is likely a limitation of inappropriate monitoring rather than a failure of the drug.20
It also appears that sugammadex should be administered based on actual body weight, particularly in the obese patient. Failure to administer a sufficient dose may result in reappearance of postoperative neuromuscular weakness (recurarization).101
 
There was an APSF newsletter a good while back that described sugammadex, and referenced literature that it binds rocuronium at 3.57 mg/mg, meaning a 200mg vial of sugammadex reverses up to ~57mg of rocuronium. Unless you need reversal to occur very rapidly, you never need to overdose this ratio as far as I can see. I always ask myself, do I think there is more than 57 mg of rocuronium still floating around his patient? I have used the medication almost exclusively as my reversal agent for over 2 years without a single PACU respiratory complication, NMB related or not. Follow the link below for that ratio information.


I’m actually kind of curious now. Someone should do a trial and see if 200mg of sugammadex reverses 50mg of rocuronium in every patient to 100%. If this exists, post it.
 
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I’m actually kind of curious now. Someone should do a trial and see if 200mg of sugammadex reverses 50mg of rocuronium in every patient to 100%. If this exists, post it.

Yeah I’ll keep an eye out. The thing is, I don’t care how fat somebody is. If I gave them 50 mg roc, I gave them 50 mg roc, period. There is no reason to suspect something significantly clinically different would occur with my sugammadex. If they were fat when I gave roc, they’re still fat when I give sugammadex. The molecular interaction doesn’t know or care care how fat the person is. I don’t use this logic for all drugs, but in this case we’re talking about a specific 1:1 molecular binding ratio, with two water-soluble drugs that have every reason to go into the same compartments. So if I’m not in any hurry, why would I overdose the known ratio? Used it 500-1000 times with no PACU complications.
 
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Yeah I’ll keep an eye out. The thing is, I don’t care how fat somebody is. If I gave them 50 mg roc, I gave them 50 mg roc, period. There is no reason to suspect something significantly clinically different would occur with my sugammadex. If they were fat when I gave roc, they’re still fat when I give sugammadex. The molecular interaction doesn’t know or care care how fat the person is. I don’t use this logic for all drugs, but in this case we’re talking about a specific 1:1 molecular binding ratio, with two water-soluble drugs that have every reason to go into the same compartments. So if I’m not in any hurry, why would I overdose the known ratio? Used it 500-1000 times with no PACU complications.

If you’re not in any hurry, I would stick with recommended best practices including objective neuromuscular monitoring and evidence based doses rather than anecdotal evidence until other doses are proven safe. Why? See above. You may be right. If you only give 50mg of roc, 200 sugammadex may be enough. I personally have a feeling it wouldn’t be if you gave 200mg of sugammadex 10 minutes after 50mg of roc for a quick case but i very well could be wrong. I would experiment myself out of curiousity but we don’t have TOF monitors with twitch percent read outs at my current practice. In any event, I wouldn’t exactly call airway shenanigans all that rare. Glad I’m MD only with a supportive anesthesia department and laid back pharmacy.
 
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If you’re not in any hurry, I would stick with recommended best practices including objective neuromuscular monitoring and evidence based doses rather than anecdotal evidence until other doses are proven safe. Why? See above. You may be right. If you only give 50mg of roc, 200 sugammadex may be enough. I personally have a feeling it wouldn’t be if you gave 200mg of sugammadex 10 minutes after 50mg of roc for a quick case but i very well could be wrong. I would experiment myself out of curiousity but we don’t have TOF monitors with twitch percent read outs at my current practice. In any event, I wouldn’t exactly call airway shenanigans all that rare. Glad I’m MD only with a supportive anesthesia department and laid back pharmacy.

Evidence/studies often lag behind logic. That’s the benefit of experience and having brains, we can make our own decisions. An interesting thought experiment is how would you feel about mixing 200 mg sugammadex with 50 mg rocuronium in one syringe, then injecting it into a patient who is spontaneously breathing with an LMA? I’ll bet nothing happens. This is what I am saying happens inside the patient too, it’s just that the patient is a “larger vial”. Since I expect those drugs to occupy similar compartments, and I’m “not in a hurry,” it’s an apt comparison.
 
I was under the impression that 4 mg of suggamadex binds 1 mg of roc in vitro, so 200 for 50 should definitely work for in vitro where there is active metabolization of the roc going on...
 
Each molecule is not on a “seek and bind” mission. That is magical thinking.

However, you will have most of that clinically relevant binding occur over a relatively short period of time, as discussed above. Similar compartments, concentration gradients and all of that.

I have quantitative twitch monitoring, which I have used many times (except when feeling lazy) with roc/sugammadex. We switched to nearly 100% use of suggamadex within a month of approval in US.

Except for the very few times I have needed action within minutes of giving roc, a single 200 mg vial has been more than enough to reverse the vast majority of patients to a TOF ratio >0.9. I do not, however use >50 mg initially very often, and always dose further roc based on twitch return. I don’t give another 50 mg of roc because the surgeon says they are tight or because I don’t want to have to worry about it for another hour.

I suspect using 100 mg in most cases would get you to a similar spot as using neostigmine.
You can always check twitches and give additional.

The reason to limit dose would be that side effects appear to be somewhat dose dependent. Plus cost, although until they start offering 100mg bottles it is unlikely to matter (assuming your pharmacy won’t split 500 mg vials into 100 mg doses).
—————-
All that said, in the case originally presented, I would be curious how much roc was given during case, when and what the last dose was, whether any twitches were checked before doses, how much suggamadex was given, and what the TOF ratio was at extubation. My feeling without those numbers is that someone possibly got a little sloppy on the long case and was giving larger doses of roc at a time, leading to a buildup/deeper than needed blockade, then doses the suggamadex based on weight. Then you have a slightly relaxed patient in PACU who tired out. Extra suggamadex gets the rest of the roc picked up and you have improvement.

I could be way off reality though, but that seems more likely than suggamadex/roc binding breaking down or a hidden central compartment.

Edit: Just found funks response about 2/kg after 4/4 twitches.
Checking twitches at some point post reversal should be standard practice, especially in these very long cases. That was well established back when we used to use that nasty neo/glyco combo, and just because we have a drug that works most of the time doesn’t mean we should skip steps.
I would go that route before changing dose of suggamadex used. If I routinely had/heard of situations where patients dropped TOF ratios in PACU then I would evolve my thinking on this and agree about needing a different dosing practice.
 
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To the person above asking about giving 200mg 10 min after 50 mg of roc, it takes longer than you want to wait for the effect you want. You need a higher dose due to the mixing required to occur in the body.

It is far different from the patient just being a big vial.
 
To the person above asking about giving 200mg 10 min after 50 mg of roc, it takes longer than you want to wait for the effect you want. You need a higher dose due to the mixing required to occur in the body.

It is far different from the patient just being a big vial.

It sounds like you’re responding to someone else, but also sort of to me with your last sentence, so I feel I have to respond. The patient being analogous to a large vial IS true if you’re “not in a hurry,” which is how I framed my point multiple times... the vial analogy is only untrue when you ARE in a hurry (hence massive dosing for emergency can’t intubate/ventilate conditions).
 
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Each molecule is not on a “seek and bind” mission. That is magical thinking.

However, you will have most of that clinically relevant binding occur over a relatively short period of time, as discussed above. Similar compartments, concentration gradients and all of that.

I have quantitative twitch monitoring, which I have used many times (except when feeling lazy) with roc/sugammadex. We switched to nearly 100% use of suggamadex within a month of approval in US.

Except for the very few times I have needed action within minutes of giving roc, a single 200 mg vial has been more than enough to reverse the vast majority of patients to a TOF ratio >0.9. I do not, however use >50 mg initially very often, and always dose further roc based on twitch return. I don’t give another 50 mg of roc because the surgeon says they are tight or because I don’t want to have to worry about it for another hour.

I suspect using 100 mg in most cases would get you to a similar spot as using neostigmine.
You can always check twitches and give additional.

The reason to limit dose would be that side effects appear to be somewhat dose dependent. Plus cost, although until they start offering 100mg bottles it is unlikely to matter (assuming your pharmacy won’t split 500 mg vials into 100 mg doses).
—————-
All that said, in the case originally presented, I would be curious how much roc was given during case, when and what the last dose was, whether any twitches were checked before doses, how much suggamadex was given, and what the TOF ratio was at extubation. My feeling without those numbers is that someone possibly got a little sloppy on the long case and was giving larger doses of roc at a time, leading to a buildup/deeper than needed blockade, then doses the suggamadex based on weight. Then you have a slightly relaxed patient in PACU who tired out. Extra suggamadex gets the rest of the roc picked up and you have improvement.

I could be way off reality though, but that seems more likely than suggamadex/roc binding breaking down or a hidden central compartment.

Edit: Just found funks response about 2/kg after 4/4 twitches.
Checking twitches at some point post reversal should be standard practice, especially in these very long cases. That was well established back when we used to use that nasty neo/glyco combo, and just because we have a drug that works most of the time doesn’t mean we should skip steps.
I would go that route before changing dose of suggamadex used. If I routinely had/heard of situations where patients dropped TOF ratios in PACU then I would evolve my thinking on this and agree about needing a different dosing practice.
We have 200mg (2ml) vials.
 
Each molecule is not on a “seek and bind” mission. That is magical thinking.

However, you will have most of that clinically relevant binding occur over a relatively short period of time, as discussed above. Similar compartments, concentration gradients and all of that.

I have quantitative twitch monitoring, which I have used many times (except when feeling lazy) with roc/sugammadex. We switched to nearly 100% use of suggamadex within a month of approval in US.

Except for the very few times I have needed action within minutes of giving roc, a single 200 mg vial has been more than enough to reverse the vast majority of patients to a TOF ratio >0.9. I do not, however use >50 mg initially very often, and always dose further roc based on twitch return. I don’t give another 50 mg of roc because the surgeon says they are tight or because I don’t want to have to worry about it for another hour.

I suspect using 100 mg in most cases would get you to a similar spot as using neostigmine.
You can always check twitches and give additional.

The reason to limit dose would be that side effects appear to be somewhat dose dependent. Plus cost, although until they start offering 100mg bottles it is unlikely to matter (assuming your pharmacy won’t split 500 mg vials into 100 mg doses).
—————-
All that said, in the case originally presented, I would be curious how much roc was given during case, when and what the last dose was, whether any twitches were checked before doses, how much suggamadex was given, and what the TOF ratio was at extubation. My feeling without those numbers is that someone possibly got a little sloppy on the long case and was giving larger doses of roc at a time, leading to a buildup/deeper than needed blockade, then doses the suggamadex based on weight. Then you have a slightly relaxed patient in PACU who tired out. Extra suggamadex gets the rest of the roc picked up and you have improvement.

I could be way off reality though, but that seems more likely than suggamadex/roc binding breaking down or a hidden central compartment.

Edit: Just found funks response about 2/kg after 4/4 twitches.
Checking twitches at some point post reversal should be standard practice, especially in these very long cases. That was well established back when we used to use that nasty neo/glyco combo, and just because we have a drug that works most of the time doesn’t mean we should skip steps.
I would go that route before changing dose of suggamadex used. If I routinely had/heard of situations where patients dropped TOF ratios in PACU then I would evolve my thinking on this and agree about needing a different dosing practice.
Each molecule is not on a “seek and bind” mission. That is magical thinking.

However, you will have most of that clinically relevant binding occur over a relatively short period of time, as discussed above. Similar compartments, concentration gradients and all of that.

I have quantitative twitch monitoring, which I have used many times (except when feeling lazy) with roc/sugammadex. We switched to nearly 100% use of suggamadex within a month of approval in US.

Except for the very few times I have needed action within minutes of giving roc, a single 200 mg vial has been more than enough to reverse the vast majority of patients to a TOF ratio >0.9. I do not, however use >50 mg initially very often, and always dose further roc based on twitch return. I don’t give another 50 mg of roc because the surgeon says they are tight or because I don’t want to have to worry about it for another hour.

I suspect using 100 mg in most cases would get you to a similar spot as using neostigmine.
You can always check twitches and give additional.

The reason to limit dose would be that side effects appear to be somewhat dose dependent. Plus cost, although until they start offering 100mg bottles it is unlikely to matter (assuming your pharmacy won’t split 500 mg vials into 100 mg doses).
—————-
All that said, in the case originally presented, I would be curious how much roc was given during case, when and what the last dose was, whether any twitches were checked before doses, how much suggamadex was given, and what the TOF ratio was at extubation. My feeling without those numbers is that someone possibly got a little sloppy on the long case and was giving larger doses of roc at a time, leading to a buildup/deeper than needed blockade, then doses the suggamadex based on weight. Then you have a slightly relaxed patient in PACU who tired out. Extra suggamadex gets the rest of the roc picked up and you have improvement.

I could be way off reality though, but that seems more likely than suggamadex/roc binding breaking down or a hidden central compartment.

Edit: Just found funks response about 2/kg after 4/4 twitches.
Checking twitches at some point post reversal should be standard practice, especially in these very long cases. That was well established back when we used to use that nasty neo/glyco combo, and just because we have a drug that works most of the time doesn’t mean we should skip steps.
I would go that route before changing dose of suggamadex used. If I routinely had/heard of situations where patients dropped TOF ratios in PACU then I would evolve my thinking on this and agree about needing a different dosing practice.

Thank you for the very thoughtful post.

- 8 hour case
- 450mg (!) roc given, 20-50mg boluses, by report bc patient was breathing each time
- last roc dose something like an hour before sug
- 2/kg sug given for 4/4 TOF, no post sug twitches "tidal volumes ok" at extubation
- no quantitative TOF (cmon man!) :D

I mean... this boils down to post-reversal TOF and sustained 5sec tetany as likely to be TOF ratio > 0.8-0.9 right?
 
Yeah I’ll keep an eye out. The thing is, I don’t care how fat somebody is. If I gave them 50 mg roc, I gave them 50 mg roc, period. There is no reason to suspect something significantly clinically different would occur with my sugammadex. If they were fat when I gave roc, they’re still fat when I give sugammadex. The molecular interaction doesn’t know or care care how fat the person is. I don’t use this logic for all drugs, but in this case we’re talking about a specific 1:1 molecular binding ratio, with two water-soluble drugs that have every reason to go into the same compartments. So if I’m not in any hurry, why would I overdose the known ratio? Used it 500-1000 times with no PACU complications.
Suggamadex does not occupy the same compartments as rocuronoum. Suggamadex does not leave the plasma, it only encapsulates rocuronoum in the blood. The effect requires rocuronoum to leave the neuromuscular junction and whatever other compartment it is distributed in, driven by a concentration gradient, and enter the plasma where it binds with suggamadex. This takes longer to occur with a deep block because more roc is distributed in these various compartments.
 
Suggamadex does not occupy the same compartments as rocuronoum. Suggamadex does not leave the plasma, it only encapsulates rocuronoum in the blood. The effect requires rocuronoum to leave the neuromuscular junction and whatever other compartment it is distributed in, driven by a concentration gradient, and enter the plasma where it binds with suggamadex. This takes longer to occur with a deep block because more roc is distributed in these various compartments.

fake news?

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There is very little information regarding the use of sugammadex in patients who are pregnant. Sugammadex appears to be effective and have a low maternal side effect profile when administered during cesarean delivery.[30][31] Sugammadex may predispose to skeletal teratogenicity. There has not been evidence of teratogenicity in humans administered up to 16 mg/kg or in rats administered six times the maximum recommended human dose (16 mg/kg). However, pregnant rabbits administered sugammadex at double the maximum recommended human dose delivered low birth weight progeny. In addition, progeny born to pregnant rabbits administered sugammadex at eight times the maximum recommended human dose had incomplete foot and sternum ossification. It is plausible that sugammadex caused this incomplete ossification. Sugammadex has been shown to remain in areas of active mineralization long after it has been eliminated from plasma—the half-life of sugammadex in bone is 172 days.


 
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