Teaching points: Defasciculating Doses

[LostTommyGuns]

A friend mentioned the use of a defasciculating dose of a nondepolarizing muscle relaxant to eliminate the fasciculations that come with using Succinylcholine (in this case they wanted no fascic. to prevent transient rises in ICP for a neuro case). After discussing it I decided that I didn't understand the mechanism for how this would work.

I can see how depolarizers work: mimic ACh to cause the endplate to generate an action potential, but whereas ACh releases the receptor, Sux. holds on and maintains end-plate depolarization. Which means the muscle contracts then becomes flaccid... So... if you give a "defasciculating dose" of Roc or Vec or whatever, it will competitively inhibit sux from binding, which means that you'll have to an increased dose of Sux... Which seems to leave you in the same situation - overriding ACh (and now Roc as well) in order to create an endplate depolarization... and fasciculations?

Clearly I'm missing something. The only thing I can think of is that by using a nondepolarizing muscle relaxant first you paralyze some muscles fibers through nondepolarization, then others through depolarization. Since you give a larger dose of Sux, it ultimately outcompetes the Roc, but over a longer time which creates smaller/less fasciculations? 😕

---

Members don't see this ad.

 

[Induc(junc)tion]

Just a fourth year medical student here with a couple of rotations under my belt, but I'll chime in. Anyways, I had an attending explain it to me like this. For a defasciculating dose, you would give about 1/10 of the intubating dose of a nondepolarizer. So say for vec, instead of 0.1 mg/kg, you would give 0.01 mg/kg right before the sux. The sux dose would remain the same. The vec would block enough receptors at the motor endplate to prevent fasciculations, but not enough to prevent the sux from doing its job.

 

[Amik25]

Just a fourth year medical student here with a couple of rotations under my belt, but I'll chime in. Anyways, I had an attending explain it to me like this. For a defasciculating dose, you would give about 1/10 of the intubating dose of a nondepolarizer. So say for vec, instead of 0.1 mg/kg, you would give 0.01 mg/kg right before the sux. The sux dose would remain the same. The vec would block enough receptors at the motor endplate to prevent fasciculations, but not enough to prevent the sux from doing its job.

According to most anesthesia textbooks, you do not give the same dose of Sux if you pre-treat with a nondepolarizer. You need to increase the dose of Sux by about 50% (In Miller, although I think in Baby Miller it says 70%).

 

[TIVA]

Myths, my friends, they're all myths.

Succinycholine does not increase ICP. It's purely theoretical. Studies in primates and in humans show no clinically significant increase in ICP from use of sux or the fasciculations from sux.

What increases ICP? Laryngoscopy.

So if you want to intubate a patient with head injury or with increased ICP and you don't want to raise they're ICP during intubation, they have to be adequately (read: deeply) anesthetized. For this, narcotics are the best, particularly the short-acting synthetic variants like fentanyl or remifentanil.

Now, sux does cause a transient rise in intra-ocular pressure, but is it clinically significant? That's a different question. Whatever rise there is in IOP is extremely short-lived (normal IOP is about 5-8 mmHg, and sux will increase it for a second or two to about 12-15 mmHg). Thus, the quandary with full stomach/open eye.

Similarly, sux also causes a transient rise in gastric pressure, which could theoretically increase the risk of aspiration. But will it lead directly to aspiration? Doubtful. I'd like to say no but I'm sure someone out there will swear they saw a case of aspiration secondary to sux, even in the face of inadequate anesthetic depth prior to intubation, trying to intubate before complete relaxtion, or someone who would've regurgitated anyway (i.e. foreign body esophagus, upper GI dysmotility, etc.)

So where did this concept of a defasciculating dose arise from? It rose from wanting to prevent the post-operative myalgias which sux can induce. And these sux-related post-operative myalgias are in fact very real and very bothersome. In fact, for some patients, they can last a good several weeks if not months. Often they will report that the worst thing about they're perioperative experience was the long persistence of muscle aches/pains. One anesthesia attending here was so debilitated by it that she had to take time off to recover; thus she almost never uses sux now.

This leads us to the next question? Does the defasciculating dose work? Does it prevent sux-induced muscle pain? Studies indicate that there is no statistical or clinical benefit. But then again, most people who are giving sux are probably giving it for purposes of rapid sequence intubation. And thus, these same people (myself included cuz I know I'm guilty of it as well), are probably not giving the "defasciculating dose" a full 3 minutes to work. Instead, we give our 1 mg of vec, wait 20-30 seconds, and then follow it with propofol and sux. And then we wonder why we still see fasciculations.

So if I could pass along just one take home point:

Sux doesn't increase ICP, laryngoscopy does. Therefore, make sure your patient is nicely anesthetized before manipulating that airway.

 

[The_Sensei]

Does the defasciculating dose work? Does it prevent sux-induced muscle pain?

No. The only thing proven to decrease the incidence of sux induced post operative myalgias is lidocaine 1mg/kg IV prior to induction. Has to do with blocking the Na channels.

 

[pgg]

And these sux-related post-operative myalgias are in fact very real and very bothersome. In fact, for some patients, they can last a good several weeks if not months.

Once upon a time a big fat dude stepped on my arm and gave me an awful comminuted fracture.

The whole-body post-op myalgia I endured for the first 48 hours s/p my ORIF were worse than the pain of feeling my radius and ulna crunched. I had the surgery a week after the injury - a week during which I went to class, and functioned more or less normally. The week after my surgery I was utterly incapacitated.

This was in my undergrad days, long before I'd ever heard of succinylcholine, so I thought maybe I'd arrested on the table and they'd done CPR by banging on my chest with a sledgehammer, with an ex-NFL-field-goal-kicker kicking my arms and legs for good measure. At my first postop appointment, the orthopod told me the myalgias were most likely from the muscle relaxant. Didn't really clue in on how that explained my pain until I saw a patient fasciculating for the first time.

No. The only thing proven to decrease the incidence of sux induced post operative myalgias is lidocaine 1mg/kg IV prior to induction. Has to do with blocking the Na channels.

Interesting ... and surprising. This forum teaches me something every day.

 

[johankriek]

and its ladies deconditioned who get it mostly.... not young muscular guys so thats an argument against using succinylcholine... i would suppose.....

 

[Laryngospasm]

Waste O' time.🙂

 

[bubalus]

No. The only thing proven to decrease the incidence of sux induced post operative myalgias is lidocaine 1mg/kg IV prior to induction. Has to do with blocking the Na channels.

1: Anesthesiology. 2005 Oct;103(4):877-84. Links

Prevention of succinylcholine-induced fasciculation and myalgia: a meta-analysis of randomized trials.Schreiber JU, Lysakowski C, Fuchs-Buder T, Tramer MR.
Department of Anesthesiology and Critical Care Medicine, University Hospital of the Saarland, Homburg, Germany. [email protected]

Fifty-two randomized trials (5,318 patients) were included in this meta-analysis. In controls, the incidence of fasciculation was 95%, and the incidence of myalgia at 24 h was 50%. Nondepolarizing muscle relaxants, lidocaine, or magnesium prevented fasciculation (number needed to treat, 1.2-2.5). Best prevention of myalgia was with nonsteroidal antiinflammatory drugs (number needed to treat, 2.5) and with rocuronium or lidocaine (number needed to treat, 3). There was a dose-dependent risk of blurred vision, diplopia, voice disorders, and difficulty in breathing and swallowing (number needed to harm, < 3.5) with muscle relaxants. There was evidence of less myalgia with 1.5 mg/kg succinylcholine (compared with 1 mg/kg). Opioids had no impact. Succinylcholine-induced fasciculation may best be prevented with muscle relaxants, lidocaine, or magnesium. Myalgia may best be prevented with muscle relaxants, lidocaine, or nonsteroidal antiinflammatory drugs. The risk of potentially serious adverse events with muscle relaxants is not negligible. Data that allow for a risk-benefit assessment are lacking for other drugs.

It was on the written boards this year.

 

[agammaglobulin]

I had a couple questions about this. If fasciculations are not the cause of myalgias after Succ admin, and the purpose of pre-treatment with non-depolarizer is to prevent fasciculations, what is the purpose of pre-treatment with non-depol? So the OR staff doesn't see the patient fasciculating? Also, what are the known risk factors for post-op myalgias? I always hear muscle bulk (young, strong men) as high risk, but apparently this isn't supported.

 

[epidural man]

1: Anesthesiology. 2005 Oct;103(4):877-84. Links

Prevention of succinylcholine-induced fasciculation and myalgia: a meta-analysis of randomized trials.Schreiber JU, Lysakowski C, Fuchs-Buder T, Tramer MR.
Department of Anesthesiology and Critical Care Medicine, University Hospital of the Saarland, Homburg, Germany. [email protected]

Fifty-two randomized trials (5,318 patients) were included in this meta-analysis. In controls, the incidence of fasciculation was 95%, and the incidence of myalgia at 24 h was 50%. Nondepolarizing muscle relaxants, lidocaine, or magnesium prevented fasciculation (number needed to treat, 1.2-2.5). Best prevention of myalgia was with nonsteroidal antiinflammatory drugs (number needed to treat, 2.5) and with rocuronium or lidocaine (number needed to treat, 3). There was a dose-dependent risk of blurred vision, diplopia, voice disorders, and difficulty in breathing and swallowing (number needed to harm, < 3.5) with muscle relaxants. There was evidence of less myalgia with 1.5 mg/kg succinylcholine (compared with 1 mg/kg). Opioids had no impact. Succinylcholine-induced fasciculation may best be prevented with muscle relaxants, lidocaine, or magnesium. Myalgia may best be prevented with muscle relaxants, lidocaine, or nonsteroidal antiinflammatory drugs. The risk of potentially serious adverse events with muscle relaxants is not negligible. Data that allow for a risk-benefit assessment are lacking for other drugs.

It was on the written boards this year.

Thanks...beat me to it.

So - teaching point - or take home point.

When someone says something on this board - "doesn't work", or " this was the only thing that proves such and such" - your tingly spider sense should go off and scholar.google.com should be wizzing in the background.

What I have always found interesting about sux induced myalgias - is that BIGGER doses decrease the incidence. I love that....and I love to pass it on to residents who probably don't believe me when I say it anyway.

finally, someone mentioned that opiods blunt ICP and also mentioned it that it was the only thing that blunted it.

So question for people who don't want to just learn and pass on DOGMA that we all pass around -

Do opioids blunt laryngoscopy sympathetic response? if so - prove it with literature. What dose is required? Perhaps the reason we have been told this is actually that it does. Perhaps it is like the dogma that opioids cause muscle rigidity.

Are there other drugs in your drawer that blunt the sympathetic response?

Is it possible to blunt the sympathetic response, yet still raise ICP? If you effectively blunt sympathetic outflow from laryngoscopy, can you still have increased ICP?

 

[pgg]

It's fun to see a thread bumped and read something I wrote 8 years ago.


These days, I reduce the risk of succinylcholine myalgias by almost never using succinylcholine.

 

[deleted162650]

Perhaps it is like the dogma that opioids cause muscle rigidity.

Sorry dude, but that's not dogma. It is a very real phenomenon that I have personally seen/caused more than once. I'll agree that it's uncommon, and that it takes large doses to cause it, but it happens. In residency we would use a narcotic based technique for crani's - titrating fent right up to the edge of apnea. Often 750-1000mcg. Every once in a while a pt would get rigid and I'm not talking about "oh they're a little difficult to ventilate" I'm talking about full body muscle rigidity. Easily resolves w/ induction and paralysis though.

 

[risnwb]

Sorry dude, but that's not dogma. It is a very real phenomenon that I have personally seen/caused more than once. I'll agree that it's uncommon, and that it takes large doses to cause it, but it happens. In residency we would use a narcotic based technique for crani's - titrating fent right up to the edge of apnea. Often 750-1000mcg. Every once in a while a pt would get rigid and I'm not talking about "oh they're a little difficult to ventilate" I'm talking about full body muscle rigidity. Easily resolves w/ induction and paralysis though.

Large doses of remifentanil for induction frequently cause rigidity. Opioid induced chest wall rigidity is certainly a real and not that uncommon phenomenon.

 

[deleted171991]

These days, I reduce the risk of succinylcholine myalgias by almost never using succinylcholine.

That's almost like saying: I haven't been sued for malpractice... since I stopped practicing medicine. 😛

 

[Planktonmd]

The idea of opiate induced muscle rigidity has been discussed and debated back and forth over the years... I am not sure there is enough evidence to support it though.

 

[risnwb]

The idea of opiate induced muscle rigidity has been discussed and debated back and forth over the years... I am not sure there is enough evidence to support it though.

Give someone a mg of remi on induction and tell me it's up for debate...

 

[Arch Guillotti]

Give someone a mg of remi on induction and tell me it's up for debate...

Did you give a mg dose of remi on purpose?

 

[pgg]

That's almost like saying: I haven't been sued for malpractice... since I stopped practicing medicine. 😛

That only works if you pay your tail premium. 🙂


I used succinylcholine about a week ago. 20 mg for laryngospasm. It worked. Myalgias weren't my chief concern at the moment. I'll also use it for RSIs when an RSI is indicated.

 

[pgg]

Give someone a mg of remi on induction and tell me it's up for debate...

The muscles that get rigid are the vocal cord adductors ...

 

[deleted162650]

. . .and biceps/triceps/quads/etc. I've seen a pt get almost into a decorticate posture before the relaxant kicked in. VC muscle contraction causes that little cough you see after a couple cc's of fent pre-induction.

 

[risnwb]

Did you give a mg dose of remi on purpose?

Not since I've been practicing under my own license 😉... Crazy attendings during residency.

 

[Planktonmd]

Sometimes people tend to perceive things according to their own existing beliefs.
In other words someone who wants to believe in muscle rigidity would see stiff people everywhere.

 

[nimbus]

Sometimes people tend to perceive things according to their own existing beliefs.
In other words someone who wants to believe in muscle rigidity would see stiff people everywhere.

Confirmation bias

 

[dhb]

Muscle rigidity exists, mostly described in the peds population, "chest wall rigidity" or what i would call "having a hard time bagging the patient" is the result of vocal cords closure.
As a side note i found there is an indirect correlation between the belief of "chest wall rigidity" and the anesthesiologists ability

 

[epidural man]

Sorry dude, but that's not dogma. It is a very real phenomenon that I have personally seen/caused more than once. I'll agree that it's uncommon, and that it takes large doses to cause it, but it happens. In residency we would use a narcotic based technique for crani's - titrating fent right up to the edge of apnea. Often 750-1000mcg. Every once in a while a pt would get rigid and I'm not talking about "oh they're a little difficult to ventilate" I'm talking about full body muscle rigidity. Easily resolves w/ induction and paralysis though.

Sorry dude - it's dogma.

If it isn't - try to prove it - because every time someone does, they have shown that difficulty masking the patient had nothing to do with chest wall or diaphragm muscle contraction. The idea is actually pretty silly. Have you ever heard of anyone dying from being awake, but not being able to breath because of muscle rigidity from the chest wall after a large dose of heroine?

But don't take my word, spend 10 minutes on google scholar and the answer to why it is difficult, even impossible to mask, after a large dose of opioids - it will become clearer. PGG and others have answered why - but find the answer yourself.

If you don't believe the cool studies that have proven this (and they are cool because they have some pretty damn cool science and devices to prove it) - find a study that shows that is CLEARLY from chest wall muscle contraction.

 

[dhb]

Give someone a mg of remi on induction and tell me it's up for debate...

I give 400mcg all the time for intubation, patients cough when it goes in because of the VC closure

 

[risnwb]

Muscle rigidity exists, mostly described in the peds population, "chest wall rigidity" or what i would call "having a hard time bagging the patient" is the result of vocal cords closure.
As a side note i found there is an indirect correlation between the belief of "chest wall rigidity" and the anesthesiologists ability

I mean .. If muscle rigidity exists, then chest wall muscle rigidity exists? As for isolated vocal cord abduction, I can say that on multiple occasions following large doses of remifentanil for induction, and after having some difficulty ventilating, I've taken a look with the laryngoscope and seen the cords wide open... Anecdotal I know.

As a side note, I find there is a direct correlation between being a dick on anonymous Internet forums and being a dick in real life 😉

 

[deleted162650]

Epidural Man, maybe we're talking about different things here. I never said anything about "chest wall" rigidity, nor did I say anything about a pt that's difficult to ventilate after narcs (I thought I made that pretty clear in my initial post).

As a resident, I was pretty skeptical as well. I've seen the studies that "disprove" chest-wall rigidity including the cool one where they narcotic loaded pts. w/ trachs. I conceded that narcotic induced rigidity is requires substantial doses, and that even then it has a relatively low incidence (essentially idiosyncratic), but it does happen. And just to be clear, by rigidity I mean global, tonic, invlountary muscle contraction. Just because you haven't seen it, doesn't mean it doesn't exist. Since this discussion started I've asked some of my older partners that are on the cardiac team if they have seen pt's get rigid from high dose narcotics. Guess what, they all have.

If you're gonna still tell me that narcotics can't cause "rigidity" then please offer an alternative hypothesis to the phenomenon I've described. I agree that VC contraction happens as has been mentioned, but again that's not what I'm talking about here.

And you're comment about heroin is silly.
A) I think this reaction is much much more likely to happen with the potent synthetic opioids than with the less potent narcs like heroin, morphine, etc.
B) I think you're gonna have a hard time asking addicts if they got rigid just before they went apneic and died
C) I didn't know you could take a large dose of heroine 😉

 

[Planktonmd]

I mean .. If muscle rigidity exists, then chest wall muscle rigidity exists? As for isolated vocal cord abduction, I can say that on multiple occasions following large doses of remifentanil for induction, and after having some difficulty ventilating, I've taken a look with the laryngoscope and seen the cords wide open... Anecdotal I know.

As a side note, I find there is a direct correlation between being a dick on anonymous Internet forums and being a dick in real life 😉

Do you have any peer reviewed evidence supporting your dick hypothesis???

 

[dhb]

I mean .. If muscle rigidity exists, then chest wall muscle rigidity exists? As for isolated vocal cord abduction, I can say that on multiple occasions following large doses of remifentanil for induction, and after having some difficulty ventilating, I've taken a look with the laryngoscope and seen the cords wide open... Anecdotal I know.

HAHA you're awesome!

 

[deleted171991]

No. The only thing proven to decrease the incidence of sux induced post operative myalgias is lidocaine 1mg/kg IV prior to induction. Has to do with blocking the Na channels.

Does anybody have a comment about this?

 

[Triple AAA]

At my first postop appointment, the orthopod told me the myalgias were most likely from the muscle relaxant.

Really now. A surgeon (an orthopod no less) blames anesthesia for a complication that they know nothing about and have no right to speak about, but chooses to do so anyway?Great, no surprises there. It's people like that who make our profession look bad. 👎

 

[deleted171991]

If the myalgias were generalized, what did the orthopod do wrong?

 

[Triple AAA]

If the myalgias were generalized, what did the orthopod do wrong?

Unless the surgeon spoke to the anesthesiologist and/or reviewed the record, In the end of the day, it's still just speculation. As a professional courtesy, those who are accused of incurring a complication should be the ones who explain in to the patient and defend themselves. It would be like me telling a patient that their fracture didn't heal properly or that their prosthetic joint is hurting them because of faulty surgical technique, something which I know nothing about as an anesthesiologist.

What makes this harmful is that it sets us up for litigation (potentially), especially when the surgeon does not understand the rationale for using the medications we use, whether the risk of myalgias were taken into account, etc. Is it likely that a patient would sue an anesthesiologist for fasciculation induced myalgias alone? Probably not. But it still robs us of a chance to tell our side of the story.

 

[Anthony2816]

Sorry to dig up an old thread, but I need advice:

As a retired anesthesiologist, I (1) have given every patient to whom I've given sux pretreatment with 3 mg of curare, and (2) never had a complaint of post-op fasciculation pain.

Last year I had lumbar spine surgery, and the day after surgery I experienced pain in every muscle in my body...particularly when I needed to cough. It was awful. The pain pattern exactly matched all I've read about succinylcholine post-op fasciculation pain. I contacted my anesthesiologist, and indeed she gave me succinylcholine without a nondepolarizer pretreatment.

I'm thus convinced that such pretreatment is necessary. Since d-tubocurarine was considered an ancient drug in my time, and now seems to be unavailable, what is the modern alternative? in this thread I've see other depolarizers, and lidocaine. I expect to be having another GETA surgery: What should I ask for, in terms of moderns pharmaceuticals: name and dosage?

I don't want to go through that unnecessary post-sux pain again.

 

[WholeLottaGame7]

Sorry to dig up an old thread, but I need advice:

As a retired anesthesiologist, I (1) have given every patient to whom I've given sux pretreatment with 3 mg of curare, and (2) never had a complaint of post-op fasciculation pain.

Last year I had lumbar spine surgery, and the day after surgery I experienced pain in every muscle in my body...particularly when I needed to cough. It was awful. The pain pattern exactly matched all I've read about succinylcholine post-op fasciculation pain. I contacted my anesthesiologist, and indeed she gave me succinylcholine without a nondepolarizer pretreatment.

I'm thus convinced that such pretreatment is necessary. Since d-tubocurarine was considered an ancient drug in my time, and now seems to be unavailable, what is the modern alternative? in this thread I've see other depolarizers, and lidocaine. I expect to be having another GETA surgery: What should I ask for, in terms of moderns pharmaceuticals: name and dosage?

I don't want to go through that unnecessary post-sux pain again.

Rocuronium (followed by sugammadex if they need neuromonitoring).

As an aside, it would send up major red flags if I had anyone, even a retired anesthesiologist, ask for specific dosages of drugs. I think it's fair to ask to avoid certain things (if they're reasonable), but I'm never promising anyone that I'm going to give X amount of drugs.

 

[T-burglar]

Next time you put in a preinduction lumbar drain for an aneurysm watch the CSF pressure when you give sux. Form your own opinion about what sux does to CNS pressure.

 

[T-burglar]

Chest wall rigidity isn’t a real thing. Light anesthesia and laryngospasm are however.

I too avoid myalgias by literally never using sux unless I’m having trouble with the airway in an LMA case or deep sedation, so like twice a year

 

[Arch Guillotti]

Chest wall rigidity isn’t a real thing. Light anesthesia and laryngospasm are however.

I too avoid myalgias by literally never using sux unless I’m having trouble with the airway in an LMA case or deep sedation, so like twice a year

What about bowel obstructions, etc???

 

[T-burglar]

What about bowel obstructions, etc???

I use high dose roc on any case That will be long enough for it to wear off. 100mg flushed In with 20cc of saline rapidly through a good IV paralyzes essentially instantaneously.

I also have a way of practicing that many people here will probably not agree with: I’m of the opinion that regurgitation on induction comes from the head rush of induction agent in A totally awake patient. I usually provide heavy sedation with midaz and fentanyl as they hit the room so that they are pretty out of it by the time I induce. I feel that it slows the brains reaction to the induction agent to the point where there is no reaction before they’re totally anesthetized. This is what I do even for bowel obstructions.

 

[anbuitachi]

im going to guess no one really understands the topic and half of this stuff is probably wrong. some places say pretreatment of small dose of sux before full intubation dose can also decrease post op myalgias.

 

[dhb]

I like sux when indicated but giving it to everybody to save 2min on induction is ******ed.

 

[pgg]

Last year I had lumbar spine surgery, and the day after surgery I experienced pain in every muscle in my body...particularly when I needed to cough. It was awful. The pain pattern exactly matched all I've read about succinylcholine post-op fasciculation pain. I contacted my anesthesiologist, and indeed she gave me succinylcholine without a nondepolarizer pretreatment.

I also had miserable post sux myalgias after surgery years ago. As a result I don't ever use it unless I have a genuine indication for an RSI.

I would just tell your next anesthesiologist that you had bad succinylcholine myalgias last time and ask that it not be used. It's not like you're asking for a case of sufentanil to take home as a souvenir.

 

[facted]

Give someone a mg of remi on induction and tell me it's up for debate...

In residency, we did this FREQUENTLY with certain attendings for certain cases. Didn't once see chest wall rigidity that made ventilation difficult. Must have done it at least 100 times.

 

[Arch Guillotti]

In residency, we did this FREQUENTLY with certain attendings for certain cases. Didn't once see chest wall rigidity that made ventilation difficult. Must have done it at least 100 times.

What’s the point of giving that much?

 

[Arch Guillotti]

I use high dose roc on any case That will be long enough for it to wear off. 100mg flushed In with 20cc of saline rapidly through a good IV paralyzes essentially instantaneously.

I also have a way of practicing that many people here will probably not agree with: I’m of the opinion that regurgitation on induction comes from the head rush of induction agent in A totally awake patient. I usually provide heavy sedation with midaz and fentanyl as they hit the room so that they are pretty out of it by the time I induce. I feel that it slows the brains reaction to the induction agent to the point where there is no reaction before they’re totally anesthetized. This is what I do even for bowel obstructions.

Sounds kind of weird

I am of the opinion that sux is the “gold standard”.

 

[facted]

What’s the point of giving that much?

Didn't use paralytics for intubation, small amount of prop, very stable induction. did a lot of ENT that way with remi infusion.

Interesting, albeit expensive, induction technique. Lots of ways to skin a cat.

 

[fakin' the funk]

I use high dose roc on any case That will be long enough for it to wear off. 100mg flushed In with 20cc of saline rapidly through a good IV paralyzes essentially instantaneously.

I also have a way of practicing that many people here will probably not agree with: I’m of the opinion that regurgitation on induction comes from the head rush of induction agent in A totally awake patient. I usually provide heavy sedation with midaz and fentanyl as they hit the room so that they are pretty out of it by the time I induce. I feel that it slows the brains reaction to the induction agent to the point where there is no reaction before they’re totally anesthetized. This is what I do even for bowel obstructions.

This is very not good.

 

[Psai]

I use high dose roc on any case That will be long enough for it to wear off. 100mg flushed In with 20cc of saline rapidly through a good IV paralyzes essentially instantaneously.

I also have a way of practicing that many people here will probably not agree with: I’m of the opinion that regurgitation on induction comes from the head rush of induction agent in A totally awake patient. I usually provide heavy sedation with midaz and fentanyl as they hit the room so that they are pretty out of it by the time I induce. I feel that it slows the brains reaction to the induction agent to the point where there is no reaction before they’re totally anesthetized. This is what I do even for bowel obstructions.

This sounds dumb. Why do you need 20 cc to flush? You need like 3 depending on your iv setup. Also your theory is weird and will probably burn you bad when you get there can't ventilate can't intubate situation for no advantage.