I got to admit I've never heard of those drugs, but I went and looked them up. Malignant hyperthermia I've heard of before and I already have a protocol to deal with that. I do recognize that the patient not coming out of anesthesia is pretty significant and would start with the ABCs and inform the ED before we even left in case they need more info from the CRNA.
Patient won't wake up after surgery
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Gurby
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The thing that gives me pause is that he's stable and maintaining (I assume) while on the sevo, and seems to go downhill once the sevo is stopped. I have no clue what's going on, I don't know any of these meds, I have never encountered this situation before. The patient is currently in the care of people with literally a combined 15+ years more education and training than I have (there must be at least 1 MD/DO surgeon around and the CRNA) who are very familiar with the patient and have a lot of tools available to them.
I'm extremely uncomfortable disturbing this seemingly stable situation. My instinct is that not calling medical control is a big mistake here.
I'm extremely uncomfortable disturbing this seemingly stable situation. My instinct is that not calling medical control is a big mistake here.
ERDoc
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There are only about 10 states that require CRNAs to have a supervising physician, so there is a good chance that this one is on her own. You will have a doctor there, the orthopedic surgeon who is doing the case but he probably has less experience with airway/sedation than you do. He's stable but you have to get him to the hospital and there is no way to keep him on the sevo. This is definitely a great thinking-outside-the-box case.
OP
OP
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This was my case a few weeks ago. I changed quite a few details (including the fact that I had no help around) just to make it sound a little more prehospital scenario-ish.
The problem was......wait for it........a cholinesterase deficiency, and the resulting prolonged neuromuscular blockade from succinylcholine!
Some degree of cholinesterase deficiency or dysfunction is present in around 1% of the general American population (considerably higher or lower in some ethnic groups) but only a few percent of that group has such a degree of dysfunction that it results in clinically significant prolongation of paralysis from succinylcholine. Many anesthetists go their entire career without seeing such a dramatic example as this one.
Most patients who have this do not know it until they undergo anesthesia with succinylcholine. This patient, for instance, had undergone several procedures in the past, but it's likely that he never had sux before. When he said "I wake up slowly from anesthesia" (lots of people say that and it isn't true), I'm very confident this was not what he was talking about. If this had happened before, he would have had it explained to him and been tested before now.
So here's what happened:
Anyway, I know we don't test twitches in EMS, and I know we don't usually wake people up......but if we are giving sux I think it's important to keep in mind how it works and how it's metabolized and what can go wrong with it. I vaguely remember hearing about cholinesterase deficiency when i first learned about succinylcholine years ago as a new paramedic, and just not worrying about really understanding what it meant, because it just didn't seem relevant.
Hope you guys found this interesting.
The problem was......wait for it........a cholinesterase deficiency, and the resulting prolonged neuromuscular blockade from succinylcholine!
Some degree of cholinesterase deficiency or dysfunction is present in around 1% of the general American population (considerably higher or lower in some ethnic groups) but only a few percent of that group has such a degree of dysfunction that it results in clinically significant prolongation of paralysis from succinylcholine. Many anesthetists go their entire career without seeing such a dramatic example as this one.
Most patients who have this do not know it until they undergo anesthesia with succinylcholine. This patient, for instance, had undergone several procedures in the past, but it's likely that he never had sux before. When he said "I wake up slowly from anesthesia" (lots of people say that and it isn't true), I'm very confident this was not what he was talking about. If this had happened before, he would have had it explained to him and been tested before now.
So here's what happened:
- Up until the wake-up, this case was very routine - everything from the pre-op to the block to the induction to the surgery itself. All the drugs and doses that I listed are what I actually gave and are my standard for a case like this, and 99% of the time my patients wake up easily and are very comfortable. The only thing slightly remarkable here was that his airway was MP 3 and he had a large neck, so I Glidescope'd him. No problems there.
- He never breathed during the case. I usually get them breathing on PSV not too long after induction, but he never did, and that's not a big deal or that unusual, so I thought nothing of it.
- After the case ended, when the gas was completely off and he should have been breathing well and responding, he was breathing extremely fast and shallow and was very hypertensive and was not responding at all. This was the first time that I knew something was really wrong, and I started working through differentials in my head. Gas is off - check. Flows are up - check. Narcotized? Nope - all he got was the 100 mcg of fent on induction. Local anesthetic toxicity? No; he got bupivacaine, which tends to case cardiovascular collapse. Worst-case in my mind was an intra-op stroke. He also had twitching movements in his extremities that I was afraid was seizure activity. I treated his hypertension and the twitching movements didn't stop. I considered giving versed but decided against it; his Sp02 was 100 and I figured I'd dose him with propofol in a couple of minutes if it didn't stop. A stroke seemed extremely unlikely, though. MH crossed my mind a couple times, but his Etc02 was normal and his temp was only slightly elevated. I had the OR nurse check his BG - 140. I then called for the i-Stat to check a sodium.
- About this time, the charge MDA walked by and poked his head in the door and said "you guys about to come out?" and then when he saw the patient still intubated and I was still assisting his ventilations he said "do you need anything?" I told him to come in and explained the problem. He immediately said "he looks like he's still paralyzed - didn't you reverse him?" I explained that he had never gotten a non-depolarizer - just the tiny defasiculating dose 90 minutes ago at this point. MDA wondered if maybe the 100 of sux I'd given him wasn't actually roc. I didn't in fact draw up the drugs for this case, but the likelihood of that seemed low. Even if that had happened, it should have worn off by now. I hadn't checked his twitches ever, because, again, I'd never given him anything long-acting. Residual paralysis post-op is actually not that uncommon - I'd seen weakness a handful of times, but never like this - but it almost always happens in someone who was inadequately reversed after several doses of a long-acting non-depolarizer. Anyway, I checked his twitches, and he had 4 weak twitches with tetany. MDA wanted to reverse the guy, thinking that he definitely looked partially paralyzed, and knowing that measuring twitches isn't always 100% reliable. I was very reluctant because I was not at all convinced we were on the right track, but at that moment I couldn't think of any reason not to try, so I agreed. Gave the guy a dose of edrephonium and....nothing.
- About now, one of the other CRNA's wandered in. "What are you guys screwing up?" he asks. We explained the situation and he says "sounds like a cholinesterase deficiency to me - you didn't reverse him, did you?" Crap. We hadn't thought of that.
- Knowing that the other CRNA was probably right about a cholinesterase deficiency - and also knowing that the reversal we just gave would prolong his weakness even more, I turned on the sevo at a low concentration to provide sedation, started the ventilator, and just waited. About 2.5 hours later I tried a 4th time to wake him up, and he was extubated successfully. We then watched him in PACU for several hours. MDA explained everything to the patient in detail, called the guy's primary, and wrote him a letter explaining what happened and strongly recommending that he avoid succinylcholine and get tested for a cholinesterase deficiency.
- Two weeks later the guy calls and tells us he got tested.....he had a dibucaine number <30
Anyway, I know we don't test twitches in EMS, and I know we don't usually wake people up......but if we are giving sux I think it's important to keep in mind how it works and how it's metabolized and what can go wrong with it. I vaguely remember hearing about cholinesterase deficiency when i first learned about succinylcholine years ago as a new paramedic, and just not worrying about really understanding what it meant, because it just didn't seem relevant.
Hope you guys found this interesting.
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Very interesting case and good to know that MH wasn't the issue. Cholinesterase deficiency is something I've never heard of, but makes sense.
NomadicMedic
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Great case. Thanks for sharing.
teedubbyaw
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Solid post.
ViolynEMT
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Makes me want to go on to learn and become more.
ERDoc
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Awesome scenario, thanks for sharing. Definitely not on my differential.
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Outstanding scenario, and a true learning opportunity for me! Thanks for posting this and providing follow up.
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Really well done. So as a followup, what would do you think an appropriate EMS treatment plan would be?
OP
OP
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I'm glad you guys liked the scenario.
Good question, Tigger.
Again, this was a really unusual case. But if this patient had to be transported, you would just transport him just like any other intubated patient - provide ventilation and sedation. The anesthesia provider may or may not be able to accompany you, depending on whether they have other patients. At the very least, of course, they should give you a good report and answer all of your questions, and also call the ED to let them know what is going on. If needed, they should be able to give you orders to follow during transport, and you can touch base with your MC before you leave to get their approval for those orders.
For sedation in a patient you are trying to wake up, it would be preferable to use drugs that don't have a long duration, so a propofol drip or dexemedetomidine would be much better than large boluses of versed, for instance. But if you don't have the ability to do a propofol drip, whatever you would normally use is fine.
Pain really isn't usually a big problem in the immediate post-op timeframe, so giving lots of opioid isn't necessary.
Things I can think of off the top of my head that could potentially cause EMS to have to transport from an outpatient surgery center: severe bleeding that is uncontrollable, intra-op stroke or MI or PE, severe allergic reaction to something, cardiac arrest for whatever reason. These are all really uncommon, of course, in the outpatient setting. But we all know how to manage them if we come across them.
Anything really bad and anesthesia-specific, like MH or LAST (local anesthetic systemic toxicity), or cardiac arrest due to succinylcholine, and an anesthesia provider really should accompany you, but they may not be able to. In that case just follow the anesthesia providers instructions to the extent that your protocols and MC allow.
Good question, Tigger.
Again, this was a really unusual case. But if this patient had to be transported, you would just transport him just like any other intubated patient - provide ventilation and sedation. The anesthesia provider may or may not be able to accompany you, depending on whether they have other patients. At the very least, of course, they should give you a good report and answer all of your questions, and also call the ED to let them know what is going on. If needed, they should be able to give you orders to follow during transport, and you can touch base with your MC before you leave to get their approval for those orders.
For sedation in a patient you are trying to wake up, it would be preferable to use drugs that don't have a long duration, so a propofol drip or dexemedetomidine would be much better than large boluses of versed, for instance. But if you don't have the ability to do a propofol drip, whatever you would normally use is fine.
Pain really isn't usually a big problem in the immediate post-op timeframe, so giving lots of opioid isn't necessary.
Things I can think of off the top of my head that could potentially cause EMS to have to transport from an outpatient surgery center: severe bleeding that is uncontrollable, intra-op stroke or MI or PE, severe allergic reaction to something, cardiac arrest for whatever reason. These are all really uncommon, of course, in the outpatient setting. But we all know how to manage them if we come across them.
Anything really bad and anesthesia-specific, like MH or LAST (local anesthetic systemic toxicity), or cardiac arrest due to succinylcholine, and an anesthesia provider really should accompany you, but they may not be able to. In that case just follow the anesthesia providers instructions to the extent that your protocols and MC allow.
Brandon O
Puzzled by facies
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lol at "What are you guys screwing up?" I like that guy. Great case.
Brandon O
Puzzled by facies
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Dumb question from a non-gaseous fellow like myself: by what mechanism does edrophonium reverse a depolarizing paralytic to begin with? (I was going to ask why giving it would exacerbate the situation above, but that actually makes more sense to me than the basic premise. Reversal agents confuse me.)
OP
OP
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Acetylcholine (Ach) is released from the prejunctional membrane, travels across the junction, and binds with post-junctional receptors, which generates a nerve potential and ultimately muscle movement. Ach is then hydrolyzed by acetylcholinesterase and its components are taken back up by the pre-junctional membrane and recycled.
Neuromuscular blockers work the same way as Ach.....they bind to the postjunctional receptors, but they are incapable of generating a potential (except for sux), so they just block Ach so that it cannot bind and generate a new nerve potential. So you get paralysis.
The non-depolarizing NMB's are termed competitive ligands because they compete with Ach for the binding sites, in that high enough concentrations of Ach will displace the NMB from the binding site, restoring nerve transmission (sux is different).
So that is how anticholinesterase reversal agents work: they bind to the acetylcholinesterase, which renders the enzyme unable to hydrolyzed Ach, so Ach concentrations increase, and the NMB is displaced from the postjunctional receptor.
Anticholinesterases can't reverse a depolarizing (sux) block, because sux binds more strongly with the post-junctional receptor and can't be knocked off by Ach. A sux block lasts until sux diffuses away from the receptor on its own and is then hydrolyzed by different plasma esterases.
In fact, an anticholinesterase with prolong a sux block, because the resulting increase in Ach will make it harder for sux to diffuse away from the receptor. Also because the anticholinesterases likely inhibit the action of the plasma cholinesterases that metabolize sux, to at least some degree.
Sux + an anticholinesterase has actually been used as a poor-mans long-acting paralytic, in fact.
Neuromuscular blockers work the same way as Ach.....they bind to the postjunctional receptors, but they are incapable of generating a potential (except for sux), so they just block Ach so that it cannot bind and generate a new nerve potential. So you get paralysis.
The non-depolarizing NMB's are termed competitive ligands because they compete with Ach for the binding sites, in that high enough concentrations of Ach will displace the NMB from the binding site, restoring nerve transmission (sux is different).
So that is how anticholinesterase reversal agents work: they bind to the acetylcholinesterase, which renders the enzyme unable to hydrolyzed Ach, so Ach concentrations increase, and the NMB is displaced from the postjunctional receptor.
Anticholinesterases can't reverse a depolarizing (sux) block, because sux binds more strongly with the post-junctional receptor and can't be knocked off by Ach. A sux block lasts until sux diffuses away from the receptor on its own and is then hydrolyzed by different plasma esterases.
In fact, an anticholinesterase with prolong a sux block, because the resulting increase in Ach will make it harder for sux to diffuse away from the receptor. Also because the anticholinesterases likely inhibit the action of the plasma cholinesterases that metabolize sux, to at least some degree.
Sux + an anticholinesterase has actually been used as a poor-mans long-acting paralytic, in fact.
Brandon O
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I was confused because it seemed like you were giving it to reverse the sux. But now in rereading, it sounds like it was because there was a question that perhaps you'd accidentally used roc instead, so you were empirically reversing that. That makes more sense.
NomadicMedic
I know a guy who knows a guy.
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That Roc was given instead of Sux was my first guess, waaaay back. But that was far to easy and figured it was a false flag.
I reeeeealy enjoyed this scenario.
I reeeeealy enjoyed this scenario.
This is actually a (somewhat) fairly common occurrence out here, maybe once a year or two per medic. The local outpatient surg center transports all patient that wake up outside of reasonably baseline to the receiving facility. I've personally been on two where they were extubated and still not waking up. Both were still stable and managing their own airways though.
Our transport time is about 1 minute code 2 across the campus to the ED
OP
OP
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Glad you guys liked it.
I almost didn't bother writing it up here because I didn't know if most here would find it relevant. Glad you did.
I almost didn't bother writing it up here because I didn't know if most here would find it relevant. Glad you did.