How about a case

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
Because in actual practice renal failure will prolong rocuronium and if you plan on extubating the patient you aren’t doing yourself any favors by using it in a patient was with renal failure when you have an option that doesn’t undergo renal clearance.

That isn't really true; even if it was, it wouldn't be a problem if you reversed everybody with sugammadex or neostigmine. The data is pretty solid that residual NMB is a real thing and that nearly everyone should get at least some reversal treatment. I contend that in actual practice rocuronium is just fine for patients with renal failure, and that avoidance of its use in ESRD is a lesser crime of academic dogma that ought to die alongside greater crimes like proving ventilation before giving relaxant.

Again, from the package insert: "When compared to patients with normal renal and hepatic function, the mean clinical duration is similar in patients with end-stage renal disease"

Its effect is only prolonged in patients with hepatic disease, which is unsurprising because rocuronium is metabolized in the liver and excreted in bile. There is a small portion excreted in urine, but not much. There is a much much less active metabolite that "has been rarely observed in the plasma or urine of humans" (also per the package insert). In any case, the end of its clinical effect is primarily brought about by redistribution, not metabolism or excretion.

The half-life of a dose of rocuronium in a normal patient and in a kidney transplant patient is exactly the same:

S5jQjys.png


Cis-atracurium is inferior to rocuronium in clinically relevant ways - you have to go to the fridge to get it, it has a much slower onset time, and there's no sugammadex equivalent for reversal, necessitating the use of neostigmine, a dirty drug.
 
Sharrock out of HSS published dozens of papers about “hypotensive epidural anesthesia” for total hips in the 1990s and 2000s. Their protocol included a goal MAP in the 50s with an Aline, cvp, and an epi drip so they probably dosed theirs up pretty good. Always seemed like a MRB (or maximal billing) anesthetic to me.

When I was a resident, we sometimes did THAs with an a-line and a nitroprusside infusion for controlled hypotension, to minimize blood loss. It seems so ridiculous now.
 
Curious about this statement. where i trained we had an orthopod that did 40 total joints a week, all under lidocaine epidurals +mac. had no issues completing total knees and hips with this technique. Are you implying the amount of LA required would cause too much of a sympathectomy?
No. I am implying that an epidural may be imperfect in its coverage, so it cannot be relied upon.
 
\

Cis-atracurium is inferior to rocuronium in clinically relevant ways - you have to go to the fridge to get it, it has a much slower onset time, and there's no sugammadex equivalent for reversal, necessitating the use of neostigmine, a dirty drug.

No you don't (at least not where i work....in my i guess backwards hospital in one of the wealthiest areas of the country)
I'm in no rush with these "sicker" patients
Not if you don't give too much relaxant.....and it's not like sugammadex doesn't have it's negative effects either. l distinctly remember a thread a couple months ago about brady arrests after giving it. I don't need that. Neostig/Glyco hasn't given me any problems yet

We can go back and forth about cis-atracurium all day and all night but I know for the students and residents on this board, if you written or oral board stem has an ESRD patient and cis-atracurium is one of the choices, that better be the one you choose first. It's easier to defend to an ivory tower type.
 
Using roc with esrd (ckd 4-5) in 2000-08ish was a total pia. Cis didn't get popular for nothing. And there are still places where you get the stink eye for using sugg. Roc doesn't work in anyone now, let alone renal patients.
 
Yes roc is 70% hepatically cleared right? We give it to our kidney transplants

Twigiddy neostig vs suggamadex... Suggamadex is the greatest anaesthesia drug in a generation with very few common side effects. Neostigmine is dirty and doesnt really work in comparison. I was lucky enough to use suggamadex daily for 6 months in Europe....
 
I almost agree with Noyac, at least with the idea of GA plus regional. Except that with a PASP of 81, I'd want an aortic BP much higher than 100/60, otherwise she won't perfuse that RV properly, plus the squeeze of the RV is dependent on the bulging of the LV into it. I would keep her BP (and HR) close to her home values (if known), or recent values in the chart. Probably much higher than 100/60. That's actually a rule of thumb I find very useful whenever I do cases on sick people, even "without an a-line".

Her LV should be fine, it just needs time to fill. A tachyarrhythmia may kill her, so dobutamine is not a friend here. Spontaneous ventilation while maintaining a decent pCO2 is, so I would encourage PSV, IF possible (and I would use sux, not roc, to give her a chance for SV).

Pain is also a pulmonary vasoconstrictor. The regional blocks should also help with avoiding a deep GA and maintaining SV. I would judiciously titrate in fentanyl, during the case, instead of a lot of sevo.

If possible, I would also place an LMA instead of an ETT (obese women are not like obese men, and there is obese and OBESE) if NPO allows - pre-induction gastric ultrasound may be a good idea. The less sympathetic stimulation, the better she'll do, but also the less aspiration...

This is also a case that would benefit from a PAC. Now that should generate the usual "a-line" type of discussion. 😛 If she misbehaves in any way during induction, I would place one.

I would avoid neuraxial like the plague. Single-shot spinal is out; I have never done a spinal catheter and I think the room for error is very small here. An epidural cannot be relied upon for surgical anesthesia. The only reason to do an epidural would be as part of an epidural/GA technique, instead of a regional/GA one. I disagree that dropping the afterload in a controlled fashion wouldn't be a problem. It could be a HUGE one: the moment the RV coronary perfusion goes away it could be bye-bye, so I wouldn't drop that afterload much (from her usual values). Unless one has a PAC in place, one doesn't know crap about her current PA pressures (the PASP of 81 was without the pain and stress of a femoral fracture - her PA pressures could be 100/60 as far as we know).

She should also get an IVC filter during the procedure.

tl;dr: For this patient I want to maintain the preload, maintain her usual afterload, avoid hypoxia/hypercarbia/pain, avoid (tachy)arrhythmias, maintain SV if possible, use regional blocks to avoid deep GA and the need for CV.

The usual disclaimer: I am not a cardiac anesthesiologist, just an "experimental (patho)physiologist", so educate me. 😉
The lack of tachycardia from dobutamine is the entire reason I would use it. I sure wouldn’t use dopamine.

The goal here should be to decrease PVR while maintaining SVR. If you want more BP than 100/60 then I’m fine with that. I chose 100/60 because she seemed to be doing fine at 90/50. These eisenmengers pts don’t have high SBP. They have high PBP. That is where I would focus.

I also don’t disagree with judicious fentanyl use but as you know, we don’t want her CO2 to go up much if at all. I want it in the 30’s which should be at least 10 pts less than her status quo.

If I had real issues and didn’t know where to go next, then I too would place a PAC. I would not wedge it tho. Anyone know why?
 
I guess if you wanted to get technical, instead of "high risk" for PA rupture you could say "small but significant risk".

In some cases I think there's an argument to be made for wedging it once to see how it compares with PA diastolic and PA mean. As someone correctly stated above, PVR = (mPAP - wedge)/CO. For a given mean PA pressure, a higher wedge = lower transpulmonary gradient = lower PVR, suggesting that elevated pulmonary pressures are related to high output state or, more likely in this scenario, to back-pressure from the left heart. The treatment would be diuretics, beta blockade, etc. If wedge is lower than expected and transpulmonary pressure is high, this would implicate elevated PVR as a culprit in which case the appropriate move would be a trial of pulmonary vasodilators to see if the PVR is fixed or reversible.

At least, one could do this kind of academic hand-wringing if so inclined (more of an ICU thing than an OR thing, probably). Or you could take the more sensical approach and just give a pulmonary vasodilator, then see if the ratio of mPAP / MAP changes.
 
Yes roc is 70% hepatically cleared right? We give it to our kidney transplants

Twigiddy neostig vs suggamadex... Suggamadex is the greatest anaesthesia drug in a generation with very few common side effects. Neostigmine is dirty and doesnt really work in comparison. I was lucky enough to use suggamadex daily for 6 months in Europe....

i simply don't know where this statement is coming from and the basis behind it. Ive been at my institution for 10 years and have exclusively used Neotigmine/Glycopyrrolate and between myself and my colleagues have had a RARE reintubation for weakness and I'm not sure where the "dirty" of this drug is coming from. Maybe some of you Suggamadex zealots should explain so I know what to look for in the future. Maybe I don't over relax people or maybe some of you guys on here are heavy handed with relaxant
 
i simply don't know where this statement is coming from and the basis behind it. Ive been at my institution for 10 years and have exclusively used Neotigmine/Glycopyrrolate and between myself and my colleagues have had a RARE reintubation for weakness and I'm not sure where the "dirty" of this drug is coming from. Maybe some of you Suggamadex zealots should explain so I know what to look for in the future. Maybe I don't over relax people or maybe some of you guys on here are heavy handed with relaxant

Nothing wrong with neo/glyco. It works. But . . . if you haven’t tried sugg yet, you really should. That **** is downright magical. And, with the price jacking on neostigmine is hardly more expensive.
 
How long is rocs effect prolonged in ESRD have you found? For example, an RSI dose 1.2mg/kg up front typically takes how long to wear off?


It is prolonged but I only ever use 30mg to intubate ESRD patients. It always works well enough and it’s always reversible by the end of the case.
 
Nothing wrong with neo/glyco. It works. But . . . if you haven’t tried sugg yet, you really should. That **** is downright magical. And, with the price jacking on neostigmine is hardly more expensive.
It could be mostly because I don't work in an outpatient setting. I believe we have Sugga at our place but I also believe you have to jump through a few hoops to get it in your room. Maybe that's why I've just stuck with Neo/Glyco. I just haven't seen these "dirty" things that happen with Neostigmine but maybe I blame whatever others see on soemthing else.
 
I only ever use 30mg to intubate ESRD patients. It always works well enough and it’s always reversible by the end of the case.
I'm will to bet that Roc has probably been better formulated since I trained in the dark ages of anesthesia so it may very well be that you can use it (apparently so since people seem to) but even as PGG said, when I was training you were treated like a remedial resident if you had rocuronium near an ESRD patient and I remember an Anesthesia-CCM doc who was covering to the ICU come all the way to the OR to shame us for giving it to one of our hearts with ESRD. But I'm sure times (and drug formulations) may have changed.
 
I'm will to bet that Roc has probably been better formulated since I trained in the dark ages of anesthesia so it may very well be that you can use it (apparently so since people seem to) but even as PGG said, when I was training you were treated like a remedial resident if you had rocuronium near an ESRD patient and I remember an Anesthesia-CCM doc who was covering to the ICU come all the way to the OR to shame us for giving it to one of our hearts with ESRD. But I'm sure times (and drug formulations) may have changed.


Seriously who cares which muscle relaxant you use in a heart? When I was a resident we used to intubate hearts with vecuronium, then switch over to pavulon. We also used 20mg of versed and 2mg of fentanyl...lol. I don’t do any of that any more.
 
I call it dirty because it's an intravenous nerve gas weapon that comes with a host of muscarinic side effects that are mostly (not completely) masked by glycopyrrolate. A small limitation is that you can't use it at all for dense blocks.

It would never have been used at all, except that there was literally no alternative to it. Now there is, at least for the steroid NMBDs.

I too used neo/glyco (or edro/atropine) every day for 10+ years and of course I agree that it works. Acetylcholinesterase inhibitors have a place still. They're needed for reversing cis-atracurium, but they're just objectively inferior to sugammadex if you're using rocuronium or vecuronium.
 
Seriously who cares which muscle relaxant you use in a heart? When I was a resident we used to intubate hearts with vecuronium, then switch over to pavulon. (We also used 20mg of verses and 2mg of fentanyl...lol)
They were really trying to fast-track people. I think sometimes OVERLY fast tracking. A few rouge attendings would extubate in the OR. If I can remember more I think that case I spoke off the heart was cancelled after the echo exam so they really wanted to extubate him but he had no strength. Of course there could've been other reasons, but I think what stuck out to the ICU attending was the Roc.

So yes, I trained in a crazy environment and maybe that has stuck with me
 
Sharrock out of HSS published dozens of papers about “hypotensive epidural anesthesia” for total hips in the 1990s and 2000s. Their protocol included a goal MAP in the 50s with an Aline, cvp, and an epi drip so they probably dosed theirs up pretty good. Always seemed like a MRB (or maximal billing) anesthetic to me.

Checking with a colleague at HSS, I believe they no longer perform such line-intensive anesthetics regularly for the arthroplasties. (I defer to any HSS anesthesiologists here)
 
The lack of tachycardia from dobutamine is the entire reason I would use it. I sure wouldn’t use dopamine.

The goal here should be to decrease PVR while maintaining SVR. If you want more BP than 100/60 then I’m fine with that. I chose 100/60 because she seemed to be doing fine at 90/50. These eisenmengers pts don’t have high SBP. They have high PBP. That is where I would focus.

I also don’t disagree with judicious fentanyl use but as you know, we don’t want her CO2 to go up much if at all. I want it in the 30’s which should be at least 10 pts less than her status quo.

If I had real issues and didn’t know where to go next, then I too would place a PAC. I would not wedge it tho. Anyone know why?
I had missed the 90/50 blood pressure. Then, of course, your 100/60 is appropriate.

What Eisenmenger?
 
Dobutamine doesn’t increase heart rate? I can’t say it’s a drug I’ve used a ton, but I was of the impression that like all beta one agonists, tachycardia and increased arrhythmogenicity are side effects. Please educate me if that’s not the case- not a drug I typically reach for, but if what you suggest is true (inotropy with less tachycardia) that’d be very useful
 
Dob doesnt cause tachycardia? Neostigmine has no issues and works great?
No roc in renal failure?

I dont get you guys sometimes...

These cases are common enough in our place. Mil and vaso are the agents you need to have nearby.
 
Eisenmenger is when the left to right shunt causes pulmonary hypertension so high that the shunt reverses to being a right to left...that's the gist anyway.
As @T-burglar pointed out, I know what Eisenmenger is, thank you.

Where's the shunt here? Did I miss something?
 
No shunt here. Not yet at least.

Dobutamine can cause tachycardia but not like dopamine. I think of it as more inotrope and less chronotrope. It also doesn’t increase BP like the others.
 
Dobutamine definitely causes tachycardia but it’s unlikely to be significant in the typical inotropic dose of 2.5-5 mcg/kg/min. Dob is frequently used as the sole agent in pharmacologic stress echos but usually the infusion is running at 20-30 mcg/kg/min (+- atropine 0.5mg) to get the HR above 85% max.
 
Top