Suggamadex in renal failure patients

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Urzuz said:
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.



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




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."




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.



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.



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.



Too soon 😱

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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I push zofran over one second every time. I never give zofran over 30 seconds or the preferred 2-5 min either. Does anybody do that?
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dchz said:
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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i think sugammadex is one of the safest drugs we have. the side effects are very rare.
 
Urzuz said:
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."
Click to expand...
I am not downplaying the potential complications associated with it. It's minimal if i'm being super generous. I know there is potential downside, that's always on the back of my mind, but it's VERY minimal.

The source you linked has 3 potential downsides with it: bradycardia, interaction with steroids, coagulopathy. They are minimal at best:

-Bradycardia: again, only case reports, no real evidence and no real unifying trigger. the reporting of these events only occurred after sugammadex was released in the US. The european sugammadex had no evidence of these events. Rest of the evidence here is about as good as the episode at my institution: some bradycardia concurrent with other drugs with varying degree of treatment and bradycardia. They claim this is dose-dependent, but there is 0 evidence of this being true.

-Interaction with steroids: we know this already, it chelates aminosteroids, so it has interactions with steroids. nothing new.

-Coagulopathy: minimal at best, i didn't list it in my list because it's not real:

TEG parameters with doses of sugammadex:
(0, 42, 193, 301 ug/ml corresponds with 0, 4 mg/kg, 16mg/kg, and 32mg/kg)

Sugammadex vs coagulopathy.jpg


Note even at 32mg/kg (301ug/ml): R, K, alpha angle, MA, and LY30% are ALL ACCEPTABLE VALUES. yes they are statistically significant, but this is not clinically significant.

I humbly followed your recommendation and gave the article a read. But the article didn't really add to my understanding of risks, in fact, it really argued for my point than yours - the risks are minimal.

Urzuz said:
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.
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This is logically inconsistent. There is no real evidence of bradycardia under appropriate dose of sugammadex either (or that it's even dose dependent), but you're championing it like every 10 pts is gonna get bradycardic if i gave 4mg/kg instead of 2mg/kg. What's the difference in level of evidence if 10 people wrote up case reports of using sugammadex in ESRD? But you act in real life like bradycardia is going to happen weekly but giving sugammadex in ESRD will never be safe for the patient.



I am always open and welcome to be critiqued and I will change my practice if i see good evidence. But at this point it feels like you're very entrenched in your position and grasping at straws.
 
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dchz said:
I am not downplaying the potential complications associated with it. It's minimal if i'm being super generous. I know there is potential downside, that's always on the back of my mind, but it's VERY minimal.

The source you linked has 3 potential downsides with it: bradycardia, interaction with steroids, coagulopathy. They are minimal at best:

-Bradycardia: again, only case reports, no real evidence and no real unifying trigger. the reporting of these events only occurred after sugammadex was released in the US. The european sugammadex had no evidence of these events. Rest of the evidence here is about as good as the episode at my institution: some bradycardia concurrent with other drugs with varying degree of treatment and bradycardia. They claim this is dose-dependent, but there is 0 evidence of this being true.

-Interaction with steroids: we know this already, it chelates aminosteroids, so it has interactions with steroids. nothing new.

-Coagulopathy: minimal at best, i didn't list it in my list because it's not real:

TEG parameters with doses of sugammadex:
(0, 42, 193, 301 ug/ml corresponds with 0, 4 mg/kg, 16mg/kg, and 32mg/kg)

View attachment 312574

Note even at 32mg/kg (301ug/ml): R, K, alpha angle, MA, and LY30% are ALL ACCEPTABLE VALUES. yes they are statistically significant, but this is not clinically significant.

I humbly followed your recommendation and gave the article a read. But the article didn't really add to my understanding of risks, in fact, it really argued for my point than yours - the risks are minimal.



This is logically inconsistent. There is no real evidence of bradycardia under appropriate dose of sugammadex either (or that it's even dose dependent), but you're championing it like every 10 pts is gonna get bradycardic if i gave 4mg/kg instead of 2mg/kg. What's the difference in level of evidence if 10 people wrote up case reports of using sugammadex in ESRD? But you act in real life like bradycardia is going to happen weekly but giving sugammadex in ESRD will never be safe for the patient.



I am always open and welcome to be critiqued and I will change my practice if i see good evidence. But at this point it feels like you're very entrenched in your position and grasping at straws.
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I feel like we need to agree to disagree. You are saying the risks are minimal. Though it may be a matter of semantics in your head, I am saying there are major risks but they’re extremely rare. Distinct but very important difference to me.

That being said, until you can provide evidence that dosing the drug appropriately leads to inadequate reversal/reparalyzation in certain patients (and not solely rely on numbers of reintubations at your institution without actually investigating why those patients are getting reintubated), I’m going to continue giving patients the lowest amount of drug possible to potentially (not definitely) minimize the (very rare) risks associated with the drug.

And I didn’t realize following the manufacturer’s guidelines amounts to “grasping at straws” in your mind, but ok. To me, needing to scour TEG studies and judge whether the times are clinically significant or not is more “grasping at straws.”

To make it clearer, after reading your arguments I don’t think your practice is that ludicrous or outside the standard of care in any way (as you seem to think I feel...no one is ‘championing bradycardia’...). I still feel like it’s wholly unnecessary to expose them to more of a medication that may have major complications associated with it. If you use the arguments you presented before, it seems like you should be giving patients 500 mg or maybe even 1000 mg of the drug since there is supposedly no downside and only upside to giving more.
 
dchz said:
-Bradycardia: again, only case reports, no real evidence and no real unifying trigger. the reporting of these events only occurred after sugammadex was released in the US. The european sugammadex had no evidence of these events. Rest of the evidence here is about as good as the episode at my institution: some bradycardia concurrent with other drugs with varying degree of treatment and bradycardia. They claim this is dose-dependent, but there is 0 evidence of this being true.
Click to expand...

One of my partners had this happen. Healthy teenager at an ASC. Sugammadex —> asystole. Turned out alright. Pretty sure I made a thread about it.
 
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I have given a lot of sugammadex. IMHO and based on the literature if you limit the total dose of sugammadex to less than 4 mg/kg the incidence and severity of side effects are reduced. This means I try to limit my reversal to 4 mg/kg max.

For example, I have no issues with giving 2.5-3.0 mg/kg of the drug by using the 200 mg dose. But, if I have a 30 kg patient I limit my initial dose to say 90-100 mg and keep the rest ready to use if needed. I rarely see any issue with using 2 mg/kg dose.

In order to save money I sometimes combine sugammadex with neo/glyco for full reversal. This works well too and keeps costs reasonable. For example, 120 kg patient gets 200 mg of sugammadex and 1.5/0.3 of Neo/glyco for full reversal.

I think side effects like bradycardia really start to escalate as the dosage goes up.
 
The authors believe that anaesthetists should be more attentive to the risk of haemodynamic changes occurring during and soon after sugammadex administration, especially in patients with underlying cardiovascular conditions who may be receiving medication recognised to slow the heart rate. We recommend that sugammadex should only be adminis- tered in the necessary dose and at a slow rate with full ECG monitoring in an attempt to reduce the incidence of these adverse effects. I.V. atropine and other vasoactive drugs should be readily available for use at all times. Most impor- tantly, it is our obligation to report any adverse drug events promptly to the relevant authorities. It is only in this way that we will ascertain the true incidence of the cardiac effects of sugammadex.

 
To pull a @BLADEMDA :
“The pivotal message from all these case reports is that un- expected life-threatening adverse reactions to sugammadex are infrequent. But, they do represent a serious health risk....We recommend that sugammadex should only be adminis- tered in the necessary dose and at a slow rate with full ECG monitoring in an attempt to reduce the incidence of these adverse effects.”

Much better worded and hopefully easier to understand than my posts. And another interesting point that the article touches on that I didn’t even think about is how ****ty anesthesiologists are at reporting serious adverse drug events. I’m sure the number of anecdotal stories like @SaltyDog has are high, but the vast majority probably go unreported.
 
BLADEMDA said:
I have given a lot of sugammadex. IMHO and based on the literature if you limit the total dose of sugammadex to less than 4 mg/kg the incidence and severity of side effects are reduced. This means I try to limit my reversal to 4 mg/kg max.

For example, I have no issues with giving 2.5-3.0 mg/kg of the drug by using the 200 mg dose. But, if I have a 30 kg patient I limit my initial dose to say 90-100 mg and keep the rest ready to use if needed. I rarely see any issue with using 2 mg/kg dose.

In order to save money I sometimes combine sugammadex with neo/glyco for full reversal. This works well too and keeps costs reasonable. For example, 120 kg patient gets 200 mg of sugammadex and 1.5/0.3 of Neo/glyco for full reversal.

I think side effects like bradycardia really start to escalate as the dosage goes up.
Click to expand...
Combining suggammadex with glyco/neo... what an... interesting idea...
 
MikeMerk-MtS said:
Do people actually do this? I mean, I guess it would work and the glyco might help w/ the brady and all... but do people actually do this?
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When suga first came out, I would first give neo/glyco to dialysis patients. After it doesn’t work (incomplete reversal), I would chase it with suga. Problem solved. Nowadays I just use suga.
 

The combination of sugammadex and neostigmine can reduce the dosage of sugammadex during recovery from the moderate neuromuscular blockade - PMC

Sugammadex is a novel neuromuscular reversal agent, but its associated hypersensitivity reaction and high cost have been obstacles to its widespread use. In the interest of reducing the necessary dosage of sugammadex, the reversal time of the ...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov


bmcanesthesiol.biomedcentral.com

Half dose sugammadex combined with neostigmine is non-inferior to full dose sugammadex for reversal of rocuronium-induced deep neuromuscular blockade: a cost-saving strategy - BMC Anesthesiology

Background Sugammadex reverses the effect of rocuronium more rapidly and effectively than neostigmine, at all levels of neuromuscular blockade (NMB). However, its cost is prohibitive. The combination of half dose sugammadex with neostigmine would be non-inferior to full dose sugammadex for the...
bmcanesthesiol.biomedcentral.com bmcanesthesiol.biomedcentral.com
 
MikeMerk-MtS said:
Do people actually do this? I mean, I guess it would work and the glyco might help w/ the brady and all... but do people actually do this?
Click to expand...

Gave 200 mg sugammadex but patient still clinically weak, so gave some additional neostigmine/glyco. Didn't have any more sugammadex laying around (have to get from pharmacy and it take 5 min or so).

Obviously, I'm sure plenty of have given neo glyco first and chased with sugammadwx if needed.

They work under 2 completely different pathways so will have additive effect.
 
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BLADEMDA said:
I have given a lot of sugammadex. IMHO and based on the literature if you limit the total dose of sugammadex to less than 4 mg/kg the incidence and severity of side effects are reduced. This means I try to limit my reversal to 4 mg/kg max.

For example, I have no issues with giving 2.5-3.0 mg/kg of the drug by using the 200 mg dose. But, if I have a 30 kg patient I limit my initial dose to say 90-100 mg and keep the rest ready to use if needed. I rarely see any issue with using 2 mg/kg dose.

In order to save money I sometimes combine sugammadex with neo/glyco for full reversal. This works well too and keeps costs reasonable. For example, 120 kg patient gets 200 mg of sugammadex and 1.5/0.3 of Neo/glyco for full reversal.

I think side effects like bradycardia really start to escalate as the dosage goes up.
Click to expand...

Do you sit your own cases now?
 
journals.lww.com

Profound Bradycardia and Cardiac Arrest After Sugammadex... : A&A Practice

nd, within 1 minute, developed severe, drug-resistant bradycardia followed by pulseless electrical activity arrest. Advanced cardiac life support was initiated and continued for 15 minutes before the return of spontaneous circulation. Subsequent cardiac workup showed no abnormalities. We believe...
journals.lww.com journals.lww.com

Transient Asystole after Sugammadex Administration for Immediate Reversal of Deep Blockade while on Dexmedetomidine Infusion in a Super Obese Patient

Sugammadex is increasingly used to reverse aminosteroid neuromuscular blocking agents. Dosing is calculated based on actual body weight, even for those who are obese. We report a case where a super obese patient (BMI 58.5 kg/m<sup>2</sup>) developed asystole, following coadministration with...
www.hindawi.com www.hindawi.com


Journal of Anaesthesiology Clinical Pharmacology

www.joacp.org www.joacp.org


 
I like Sugammadex and think it is an excellent drug for reversing rocuronium. That said, you need to be prepared to treat severe bradycardia if it were to occur in your patient.
 
BLADEMDA said:
I like Sugammadex and think it is an excellent drug for reversing rocuronium. That said, you need to be prepared to treat severe bradycardia if it were to occur in your patient.
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Anyone who would give suggamadex would be prepared to treat bradycardia. Also, I often hear anesthesiologists comment on using X to save money. Wouldn't that require a knowledge of what the hospital charges the patient (not simply what the drug cost the hospital) and what the patient's insurance company would 1) cover and 2) not cover and charge the patient?

Saying 'I do this to save money' is in my opinion pretty shortsighted. Suggamadex is clearly superior to Neo/glyco. Like, in every way. It's no longer debatable. Yes, we need to be prepared to treat its negative effects. Same with Neo/glyco. But giving both classes of reversal honestly doesn't make any sense.
 
Or you could just bite the bullet and give cis and accept that it’s gonna be weak because it wasn’t stored properly, but then you don’t have to deal with this nonsense.
 
dchz said:
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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Post marketing data shows that anaphylaxis incidence seems tightly correlated to dose.

I think it is a good idea to only give the recommended dose.

One of the reasons I really like Quantitative Twitch monitoring is because if they have >0.9 TOF ratio, I don’t have to give anything. I like that solution best.
 
BLADEMDA said:
Thanks. But, Sugammadex costs $90 per vial and if I can safely use other drugs to keep the costs reasonable i will do so. 2 vials of Sugammadex will cost $180. The recommendation for dosing sugammadex is actual body weight not ideal body weight.
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But wouldn't sugga save overall costs, decreased pacu pulm complications, less residual blockade etc etc. I mean is this really the one drug that will break the bank for hospital with all it's benefits...?
 
2Fast2Des said:
But wouldn't sugga save overall costs, decreased pacu pulm complications, less residual blockade etc etc. I mean is this really the one drug that will break the bank for hospital with all it's benefits...?
Click to expand...

Hospital admins don't think like that
 
A few case reports for sugammadex in roc anaphylaxis. Seen 2 of these so far but before sugg. Probably have seen my two, but anyone else?
 
dchz said:
Show me the data.

Also true anaphylaxis by definition is not dose dependent.
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Agreed, there are plenty of case reports of anaphylaxis from tiny subcutaneous injections of various drugs. I don't see why an anaphylactic reaction should be dose dependent when it's the host response that matters.
 
dchz said:
Show me the data.
Click to expand...
I will maybe. It depends.

It will take me some time, and effort - on something I care little about. You and I are on different sides of this camp. I am on the side of less is better if it does the job just as good as more. You are on the side that more is better because it may do better than giving less. If that works for you, great. I hope it doesn't cause problems. I am a true believer in the marvelous saying "You make your bed, you lie in it."

So I will do the work, IF you first tell me what the answer will do for you. Will you change your practice? Will you admit I am right? What exactly will the data do for you and why do you want me to show you the data? Was this just a request because you don't think it is there and you think I will be on a wild goose chase coming up with something that doesn't really answer the question?

Because you must have at least considered the fact that the data IS there - and so if you have already decided it doesn't matter what it shows, then I don't want to spend the time producing it.
 
MoMoGesiologist said:
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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In the new world of suggamadex, I don't check twitches. They tell me nothing. Unless you have quantitative monitoring, you have learned nothing - at least to the extend that it changes your decision making tree.

If I gave roccuronium, and I know the time to the last dose (and I understand there is HUGE variability in metabolism rate), and the patient is pulling adequate tidal volumes - I am going to reverse...I don't care if there is no twitches with 12 post tetanic twitches, 1, 2, or 4 twitches. I have no idea what the TOF ratio is - so reversing is required. If it has been 4 hours since the last dose and patient is pulling adequate tidal volumes, I'm not going to reverse.

Now, the time I WILL check, is if the patient isn't tugging on the vent at all. Then I need to decide what is going on.

And let me finally say - since I've been doing this for a while, I NEVER seem to find myself at the end of the case with zero post-tetanic twitches. THAT seems like the SLOPPY part to me if that happens.
 
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epidural man said:
If it has been 4 hours since the last dose and patient is pulling adequate tidal volumes, I'm not going to reverse.
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“Adequate tidal volumes” tells you nothing about the degree of NMB. Why 4 hours? Surely it matters how large of a total dose was given too? AFAIK 4 hours is not a data driven cutoff - you yourself acknowledged that there is massive variability in the rate at which roc is metabolized.
 
epidural man said:
So I will do the work, IF you first tell me what the answer will do for you. Will you change your practice? Will you admit I am right? What exactly will the data do for you and why do you want me to show you the data? Was this just a request because you don't think it is there and you think I will be on a wild goose chase coming up with something that doesn't really answer the question?
Click to expand...

dchz said:
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.
Click to expand...

Yep. As stated before your reply in this thread. I will do the best thing for my patients with the best evidence I have. So if you present me better evidence I will react to it accordingly.

Obviously I will give you credit for being right and teaching me something. But if I am giving you credit there I must also call out your BS:

epidural man said:
Post marketing data shows that anaphylaxis incidence seems tightly correlated to dose.
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You stated the data shows X but you don't have any proof of data showing X.

Your credibility is gonna be questionable if you make these claims without any data to back it up.
 
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Hork Bajir said:
“Adequate tidal volumes” tells you nothing about the degree of NMB. Why 4 hours? Surely it matters how large of a total dose was given too? AFAIK 4 hours is not a data driven cutoff - you yourself acknowledged that there is massive variability in the rate at which roc is metabolized.
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Yes it does. Have you ever seen someone with a fully functional diaphragm with zero twitches and les than 10 or so post-tetanic twitches?
 
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anaesthetic said:
Sorry, but the literature does not support you. This is coming from somebody who used to believe that 4 hours would be enough time for NBMDs to clear completely and thus reversal wouldn't be necessary (it's actually not true for some patients, due to variability in clearance as mentioned before).

Current Status of Neuromuscular Reversal and Monitoring: Challenges and Opportunities

Some highlights:
"Despite the widespread availability of PNSs in the ORs (76% of European departments and 97% of U.S. departments), 19% of European and 9% of U.S. clinicians never use them, and their use does not seem to always help clinicians identify residual neuromuscular weakness: more than half of clinicians incorrectly estimated the incidence of clinically significant residual block to be less than 1%.32 A survey, as well as numerous previous clinical investigations, has reported on the limitations of subjective evaluation.112 The ability to detect TOF fade by subjective (tactile) means appears to be influenced by clinical experience only marginally; anesthesiologists inexperienced in assessing tactile fade were able to identify it only when the TOF ratio was less than 0.30, while only one in five experienced anesthesiologists was able to correctly identify it when the TOF ratio was between 0.51 and 0.70.60"

"Other limitations of subjective evaluation relate to the site (muscle) that is monitored. There are well-known differences in the timecourse of responses to NMBAs at different muscle groups. Central muscles (diaphragm) recover earlier than peripheral muscles (adductor pollicis), but that does not imply that the rest of the respiratory muscles are functioning normally. Upper airway muscles critical to maintaining airway patency and protection from pulmonary aspiration of secretions or gastric contents are very sensitive to NMBAs and do not recover fully until the TOF ratio is near baseline."

"Other indicators of recovery, such as subjective assessment of lack of TOF fade, sufficient time since administration of reversal agents (or NMBA), adequate tidal volume, the presence of 5-s head lift, and so forth, cannot be used to exclude residual block and the potential for postoperative complications."
Click to expand...

I am so confused by your response. What exactly do you think my point is? And how do you think this post contradicts anything I’ve said?
 
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BLADEMDA said:

Lower doses of sugammadex may not result in clinically significant delays in recovery from neuromuscular blockade, according to a new study. A team of Belgian investigators found that the minimal optimal dose of sugammadex in elective surgery might be as low as 0.5 mg/kg.
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Always gave no more than 200 mg and if patient was real small than the I gave less at 2mg/kg.
I was at OU in 2017 where they gave it to everyone. One of their attendings said that they most often used 200 for each patient, I guess to save money overall since it is expensive and never had any issues for over a year. So I went with it.
I hardly use it now but I did give a whopping 500mg dose to a 156 kg patient when neo and glyco didn’t touch him and he had a story that made me think Pseudocholinesterase def.
 
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