#Case_04 Another dilemma of Sux

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DrAmir0078

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After my previous post, two days ago

#Case_03 Sux apnea sucks, but was it Sux?

We got a new case
90 kg male, with scheduled thyroid tumor resection. Operation lasts 3 hours (was performed by one of the elite surgeons in Iraq, very complicated with wide neck dissection, even the team was aware of any complication like brain edema and even Tracheostomy kit was standby}. The operation went well without using Tracheostomy, patient well sedated, at the end the patient starts to wake up, reversal of nmb done by administrating 2.5 mg neostigmine /1.2 Atropine. Once extubation done, the patient rapidly deteriorated, unable to breath and lock jaw happened (the later is my diagnosis)- beside tracheomalacia was differentialy diagnosed by them, his SPO2 went down to 20%, Surgeon was about to reexplore and put needle cricothyrodectomy, the Anesthesiologist and for emergency purpose gave 300 mg of Succinylcholine, the patient fully relaxed, SPO2 raised after good ventilation by Mask, and was able to tube the patient back, and the surgeon performed Tracheostomy successfully. Interestingly the patient restored spontaneous breathing after 10 minutes and once the surgery team finished Tracheostomy, patient was discharged from the OR.
So between the time of administering neostigmine/Atropine and later Succinylcholine was less than 15 minutes!
Previously in the other post, as we know there is a caution of not to administer succinylcholine after neostigmine (window time 1-2 hours)
How will you explain what happened in this case!

My explanation (If I am wrong correct me), the dose of neostigmine 2.5 mg wasn't enough to inhibit Acetylcholinestrase (partial reversal happened), as we know each Acetylcholinestrase can hydrolyze 25000 Ach molecules / seconds. This would explain the distribution of the neostigmine wasn't enough to act as AChE inhibitors [as we know the process is by oxydiaphoretic (or ‘acid-transferring’) inhibitors: act as an alternative substrate for AChE, producing a more stable carbamylated enzyme complex. Subsequent hydrolysis of the complex and thus reactivation of the enzyme is slow. - A to Z Anesthesia and Intensive care and perioperative medicine 5th edition]

So, when Succinylcholine administred, here the 300 mg, only 30 mg reached the synthetic cleft and the rest 270 mg being hydrolyzed by plasma chlinestrase aka Pseudocholinesterase. So, the remaining 30 mg was acting like competitive (its role is not competitive) at ACh-Nicotinic receptors with what left AChE who is hydrolyzing ACh. (did we induce phase II block? - this is a Benign question). So the time of dissociation of Succinylcholine from the receptor is about 10 minutes and that what happened and it was hardly and competitively replaced by ACh and although conformational changes happened, but Ach sought normal receptor first (Or both worked together, one is Succinylcholine acting on fatigue the muscles to get paralysis while Ach maintained regular exercise at the receptor - such a complexity)

So if this patient gained full recovery, in such window time, while the other patient in the previous post, the time was 3 hours and a half after the last neostigmine/atropine was given - did this will explain and address that the previous patient had scoline apnea or what? Taking into the consideration of the same dose of neostigmine 2.5 mg was given for both patients!

As first world Anesthesiologists, will you advise us to use the optimal dose of neostigmine (50 - 70 mcg/kg) not what I saw only 2.5 mg one ampoule and if something happened we can repeat the dose, but mostly 2.5 mg is enough as we have seen in our practice!

Thanks for reading, this is a scientific debate!

Amir
 
Without being there, I tend to think that a patient that gets extubated and then rapidly desats to 20% while "not breathing" has laryngospasm. Patients that are weak from incomplete reversal tend to look weak and floppy but have gradual slow desaturations. It's usually at least 5-10 minutes after extubating (or longer) that they tire out and can't keep sat up but it's a gradual process.
 
Without being there, I tend to think that a patient that gets extubated and then rapidly desats to 20% while "not breathing" has laryngospasm. Patients that are weak from incomplete reversal tend to look weak and floppy but have gradual slow desaturations. It's usually at least 5-10 minutes after extubating (or longer) that they tire out and can't keep sat up but it's a gradual process.
Indeed, it was on the dish "Laryngospasm", but what made them think of tracheomalacia is the wide spread of the tumor, plus the very long complicated procedure which obviously collapsed the trachea after extubation. Yes, the team was aware of the problem if happened. Extubation done with good eVt, but honestly because of the procedure, patient history of COPD, was expected to be floppy and Anesthesiologist was about to sedate him after extubation but rapidly deteriorated. But what to explain lockjaw like sign (very spastic that we couldn't open his mouth while desat). It happened in seconds, do you think by giving him a chance of Propofol 50 mg, will be feasibly better than giving succinylcholine?
But, hadn't solve Sux after neo issue?
 
was there any attempt to ventilate with the mask? I mean I'm sure he wasn't an easy mask ventilation in the first place but I would have tried it. If I suspect laryngospasm I usually try positive pressure ventilation first and then propofol second. If that sat goes low enough I just push the succinylcholine.
 
was there any attempt to ventilate with the mask? I mean I'm sure he wasn't an easy mask ventilation in the first place but I would have tried it. If I suspect laryngospasm I usually try positive pressure ventilation first and then propofol second. If that sat goes low enough I just push the succinylcholine.
I assure you, he was very difficult to ventilate by Mask, the exact word to describe him "locked up" can't get air in neither to open his mouth, cyanosis developed very fast!
The chance to give Propofol was abolished with the rapid catastrophic situation, so like what you said "Succinylcholine in was a must"
 
I assure you, he was very difficult to ventilate by Mask, the exact word to describe him "locked up" can't get air in neither to open his mouth, cyanosis developed very fast!
The chance to give Propofol was abolished with the rapid catastrophic situation, so like what you said "Succinylcholine in was a must"

Nasal airway? You don't need an open mouth to be able to ventilate somebody, although like I said I understand this patient may have been very difficult and not always possible.
 
This sounds like a patient that was extubated in stage II and laryngospasmed. More importantly, it sounds like this happened and he was extubated without an oral airway in.

Some people like to have a soft bite block in, but I always go for the guedel oral airway, so that if I need to I can effectively ventilate post-extubation. Granted, I’ve only had someone laryngspasm twice in the past year and a half, and I’ve burned a lot of oral airways in the interim... I guess it’s your call. Also, 300mg of succinylcholine is a heaaavy dose for laryngospasm. You could have used 20-40mg to relax the cords emergently.
 
This sounds like a patient that was extubated in stage II and laryngospasmed. More importantly, it sounds like this happened and he was extubated without an oral airway in.

Some people like to have a soft bite block in, but I always go for the guedel oral airway, so that if I need to I can effectively ventilate post-extubation. Granted, I’ve only had someone laryngspasm twice in the past year and a half, and I’ve burned a lot of oral airways in the interim... I guess it’s your call. Also, 300mg of succinylcholine is a heaaavy dose for laryngospasm. You could have used 20-40mg to relax the cords emergently.
What do you mean by stage II?

Furthermore, do you usually extubate your patients while an airway in? is it uncomfortable for awake patient? Or you manage to give Propofol prior to ensure Ventilation and prevent any possibility of laryngospasm (like almost deep extubation technique)

But do you think such dose of 0.25 mg - 1 mg / Kg (22.5 mg - 90 mg for laryngospasm) would be enough to ventilate him by Mask, and to relax his jaw so we can easily intubate him?
That sounds cool

Yet, there is no objection for using Succinylcholine after Neostigmine!
 
What do you mean by stage II?

Furthermore, do you usually extubate your patients while an airway in? is it uncomfortable for awake patient? Or you manage to give Propofol prior to ensure Ventilation and prevent any possibility of laryngospasm (like almost deep extubation technique)

But do you think such dose of 0.25 mg - 1 mg / Kg (22.5 mg - 90 mg for laryngospasm) would be enough to ventilate him by Mask, and to relax his jaw so we can easily intubate him?
That sounds cool

Yet, there is no objection for using Succinylcholine after Neostigmine!

The dose of succinylcholine for laryngospasm rarely needs to exceed 0.1 mg/kg. It is always hard to know what happened without being there.

Patients generally tolerate oral airways just fine while waking up. When they’re awake enough that it bothers them they can take it out.
 
The dose of succinylcholine for laryngospasm rarely needs to exceed 0.1 mg/kg. It is always hard to know what happened without being there.

Patients generally tolerate oral airways just fine while waking up. When they’re awake enough that it bothers them they can take it out.
We agree that Succinylcholine dose for laryngospasm, but was it?

We can't ignore the fact of the Succinylcholine storage vs efficacy over here!

The Anesthesiologist was deeply thinking of the inputs to conclude the dose required with what happened as catastrophe, I believe he wants the rapid effect of Succinylcholine to work as competitive as possible in the presence of the effect of neostigmine. (I am thinking loudly)
 
The dose of succinylcholine for laryngospasm rarely needs to exceed 0.1 mg/kg. It is always hard to know what happened without being there.

Patients generally tolerate oral airways just fine while waking up. When they’re awake enough that it bothers them they can take it out.

That guy was saying he places oral airways routinely which I think is overkill
 
There are details missing here.
When did you extubate? How long after reversal? What criteria did you use to extubate? What was tof? What was tv? What was max inspir force?


What did you.extubate him on to? What position was he? Bite block? What was fio2? Opioids?

We can't adequately answer your qs. I feel without much more detail
 
What do you mean by stage II?

Furthermore, do you usually extubate your patients while an airway in? is it uncomfortable for awake patient? Or you manage to give Propofol prior to ensure Ventilation and prevent any possibility of laryngospasm (like almost deep extubation technique)

But do you think such dose of 0.25 mg - 1 mg / Kg (22.5 mg - 90 mg for laryngospasm) would be enough to ventilate him by Mask, and to relax his jaw so we can easily intubate him?
That sounds cool

Yet, there is no objection for using Succinylcholine after Neostigmine!

Look up stage 2 Guedels stages of Anesthesia.
Clearly a case of laryngospasm with masseter spasm occurring during stage 2.


Sent from my iPhone using SDN mobile
 
There are details missing here.
When did you extubate? How long after reversal? What criteria did you use to extubate? What was tof? What was tv? What was max inspir force?


What did you.extubate him on to? What position was he? Bite block? What was fio2? Opioids?

We can't adequately answer your qs. I feel without much more detail
10 minutes after the neostigmine/atropine was given extubation done.

No TOF (welcome to the limited resources), Tidal volume = 320, MIP was acceptable

Position head up (thyroid procedure), bite block (welcome to the limited resources), FiO2 100% oxygen on 7Lt (previously discussed - we don't have closed circuit)

Opioid : Premedication / induction with Fentanyl, during the operation was on ON/Off remifentanil

Patient was pre diagnosed with tracheomalacia, wide neck dissection, manipulation of internal carotid, preoribtal edema developed during the procedure (brain edema was taken into the consideration too), mannitol was given, while during manipulation of the trachea, an NG tube was inserted to help lifting the trachea and guide the surgeon, what else to remember? Long operation time, old age, heavy smoker, COPD, by the way - he had unilateral cord paralysis, was sent for Tracheostomy, but surgeon wants to give him a chance, unfortunately ended up with Tracheostomy.

Probably, our parameters of extubation, Anesthesiologist meant to near deep extubation, and continue sedation taking into the consideration of stress. But what happened as explained.

Furthermore, we discussed with the surgeon, the patient is feeling better, and further discussed about tracheomalacia, as he said "I felt them soft, even because of the dissection - CA thyroid - he excised part of the cartilage".

The patient is going to get his tracheostomy closed very soon.
 
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Look up stage 2 Guedels stages of Anesthesia.
Clearly a case of laryngospasm with masseter spasm occurring during stage 2.


Sent from my iPhone using SDN mobile
Pre diagnosed with tracheomalacia, explained a bit more in the previous comment.

Thanks for clarification, yes we are aware of these stages.
 
"Long operation time, old age, heavy smoker, COPD, by the way - he had unilateral cord paralysis"

How many hours is long?

That's almost definite going to ICU intubated for a day or 2
 
No TOF (welcome to the limited resources), Tidal volume = 320, MIP was acceptable
Acceptable mip is not a criteria for extubating this guy at end of his op. He needs to be a shining light to be extubated for me in the OR. Definite tv over 500, obeying commands, normal istat(I didn't see abg anywhere in your story)...

It doesn't sound like this guy was a candidate to extubate for a few days post his op
 
Acceptable mip is not a criteria for extubating this guy at end of his op. He needs to be a shining light to be extubated for me in the OR. Definite tv over 500, obeying commands, normal istat(I didn't see abg anywhere in your story)...

It doesn't sound like this guy was a candidate to extubate for a few days post his op
He ended up with tracheostomy! Not a tube and ICU
3.5 hours operation time!

Yes, almost shining light, obeys commands, tv 320, good power, no istat (you know where are we? - if I hadn't worked at GWUH ER - I mean a US hospital, will never know what you are talking about - Abbot istat for Chem 8 at least or/ VBG from istat lactate, I truly miss)

ABG - Some centers have ABGs, some broken device, this one does not have !
 
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Tracheomalacia severe enough to cause airway collapse and loss with spontaneous, negative pressure inspiration is a possibility, given the size of the mass that was removed.

And a tracheostomy is sometimes the correct decision in patients who get big neck dissections for large peri-airway masses.

But I'm a little skeptical that a trach was really needed. If the obstruction was due to tracheomalacia, we would expect positive pressure ventilation by mask to be successful. Instead you could not ventilate at all, and it got better with muscle relaxant. Obstruction with PPV is not consistent with tracheomalacia. I think he probably got extubated during stage 2, as others suggested above, and had an episode of laryngospasm, which was successfully treated with succinylcholine.

Hard to really know without directly seeing what happened.
 
Tracheomalacia severe enough to cause airway collapse and loss with spontaneous, negative pressure inspiration is a possibility, given the size of the mass that was removed.

And a tracheostomy is sometimes the correct decision in patients who get big neck dissections for large peri-airway masses.

But I'm a little skeptical that a trach was really needed. If the obstruction was due to tracheomalacia, we would expect positive pressure ventilation by mask to be successful. Instead you could not ventilate at all, and it got better with muscle relaxant. Obstruction with PPV is not consistent with tracheomalacia. I think he probably got extubated during stage 2, as others suggested above, and had an episode of laryngospasm, which was successfully treated with succinylcholine.

Hard to really know without directly seeing what happened.

@pgg
Indeed, we weren't able to ventilate and the lockjaw was a problem too, the collapse and desat was rapid. So, probably was combined Laryngospasm and airway collapse with stage II extubation (although our parameters was suggested to extubate)
I will further discuss the case with the Attending !
 
I'm in a very different location to Amir, but just for my further learning;

If I'm running Remi for a neck exploration +/- everything, I typically see the patient get weaned off anaesthetic agent, with a continuing remi infusion at the end of the case --> Get them to a point where they are barely maintaining pressure demand vent and prepare for extubation--> cease remi infusion and sit them upright --> Poke them on the head until they start following commands and maintaining good MV and TV without any vent. support (but might need some reminding to breath) -> extubate while airway reflexes are still somewhat suppressed and apply some CPAP while the remi clears over the next minute or two.
I was told the reasoning behind this is to maintain suppression of airway reflexes (including coughing + laryngospasm) at the end of a neck case.

Amir, it sounds like you were giving remi on/off during the case. As infusion... or? It also sounds like all opioids were off-board at the end of the case, is this correct? Could this have contributed to the presentation? Anyone feel free to correct my thought process here?
 
That guy was saying he places oral airways routinely which I think is overkill

We get them on the cheap, so I just use them as my bite block, average BMI is probably >40 so just makes my life easier

In regards to the case, def stage 2 extubation and laryngospasm. In my practice there are only two options for this patient:
1) Go to ICU intubated and sedated to cool off for a day
2) If extubating in OR, awake AF extubation with patient informed of awake AF extubation because of their underlying comorbidities
 
We get them on the cheap, so I just use them as my bite block, average BMI is probably >40 so just makes my life easier

In regards to the case, def stage 2 extubation and laryngospasm. In my practice there are only two options for this patient:
1) Go to ICU intubated and sedated to cool off for a day
2) If extubating in OR, awake AF extubation with patient informed of awake AF extubation because of their underlying comorbidities

Why not extubate over a tube exchanger
 
Why not extubate over a tube exchanger

If you're thinking about extubating over a tube exchanger in the OR, you should probably just be taking them to the unit intubated. Also, even if you have a tube exchanger in, that still doesn't guarantee you'll be able to get a tube back in if the airway is a disaster s/p surgical manipulation.
 
I'm in a very different location to Amir, but just for my further learning;

If I'm running Remi for a neck exploration +/- everything, I typically see the patient get weaned off anaesthetic agent, with a continuing remi infusion at the end of the case --> Get them to a point where they are barely maintaining pressure demand vent and prepare for extubation--> cease remi infusion and sit them upright --> Poke them on the head until they start following commands and maintaining good MV and TV without any vent. support (but might need some reminding to breath) -> extubate while airway reflexes are still somewhat suppressed and apply some CPAP while the remi clears over the next minute or two.
I was told the reasoning behind this is to maintain suppression of airway reflexes (including coughing + laryngospasm) at the end of a neck case.

Amir, it sounds like you were giving remi on/off during the case. As infusion... or? It also sounds like all opioids were off-board at the end of the case, is this correct? Could this have contributed to the presentation? Anyone feel free to correct my thought process here?

Thanks for the comment...
The Remi dose was ON/OFF at the beginning of the surgery, it was completely off the last two hours.
 
I had one case ever of a hyperdynamic segment of trachea eventually diagnosed as tracheomalacia post-op. It was distal to my ett so I had to main stem intentionally.

That said, I feel I deal with a laryngospasm every few months.
 
After my previous post, two days ago

#Case_03 Sux apnea sucks, but was it Sux?

We got a new case
90 kg male, with scheduled thyroid tumor resection. Operation lasts 3 hours (was performed by one of the elite surgeons in Iraq, very complicated with wide neck dissection, even the team was aware of any complication like brain edema and even Tracheostomy kit was standby}. The operation went well without using Tracheostomy, patient well sedated, at the end the patient starts to wake up, reversal of nmb done by administrating 2.5 mg neostigmine /1.2 Atropine. Once extubation done, the patient rapidly deteriorated, unable to breath and lock jaw happened (the later is my diagnosis)- beside tracheomalacia was differentialy diagnosed by them, his SPO2 went down to 20%, Surgeon was about to reexplore and put needle cricothyrodectomy, the Anesthesiologist and for emergency purpose gave 300 mg of Succinylcholine, the patient fully relaxed, SPO2 raised after good ventilation by Mask, and was able to tube the patient back, and the surgeon performed Tracheostomy successfully. Interestingly the patient restored spontaneous breathing after 10 minutes and once the surgery team finished Tracheostomy, patient was discharged from the OR.
So between the time of administering neostigmine/Atropine and later Succinylcholine was less than 15 minutes!
Previously in the other post, as we know there is a caution of not to administer succinylcholine after neostigmine (window time 1-2 hours)
How will you explain what happened in this case!

My explanation (If I am wrong correct me), the dose of neostigmine 2.5 mg wasn't enough to inhibit Acetylcholinestrase (partial reversal happened), as we know each Acetylcholinestrase can hydrolyze 25000 Ach molecules / seconds. This would explain the distribution of the neostigmine wasn't enough to act as AChE inhibitors [as we know the process is by oxydiaphoretic (or ‘acid-transferring’) inhibitors: act as an alternative substrate for AChE, producing a more stable carbamylated enzyme complex. Subsequent hydrolysis of the complex and thus reactivation of the enzyme is slow. - A to Z Anesthesia and Intensive care and perioperative medicine 5th edition]

So, when Succinylcholine administred, here the 300 mg, only 30 mg reached the synthetic cleft and the rest 270 mg being hydrolyzed by plasma chlinestrase aka Pseudocholinesterase. So, the remaining 30 mg was acting like competitive (its role is not competitive) at ACh-Nicotinic receptors with what left AChE who is hydrolyzing ACh. (did we induce phase II block? - this is a Benign question). So the time of dissociation of Succinylcholine from the receptor is about 10 minutes and that what happened and it was hardly and competitively replaced by ACh and although conformational changes happened, but Ach sought normal receptor first (Or both worked together, one is Succinylcholine acting on fatigue the muscles to get paralysis while Ach maintained regular exercise at the receptor - such a complexity)

So if this patient gained full recovery, in such window time, while the other patient in the previous post, the time was 3 hours and a half after the last neostigmine/atropine was given - did this will explain and address that the previous patient had scoline apnea or what? Taking into the consideration of the same dose of neostigmine 2.5 mg was given for both patients!

As first world Anesthesiologists, will you advise us to use the optimal dose of neostigmine (50 - 70 mcg/kg) not what I saw only 2.5 mg one ampoule and if something happened we can repeat the dose, but mostly 2.5 mg is enough as we have seen in our practice!

Thanks for reading, this is a scientific debate!

Amir

How do you dose your neuromuscular blockers without a twitch monitor?? You have an ultrasound and anesthesia machine, but no twitch monitor?

Are you using only cisatracurium and ateacurium? For these long cases, do you skip residing your neuromuscular blocker for a couple hours??
 
How do you dose your neuromuscular blockers without a twitch monitor?? You have an ultrasound and anesthesia machine, but no twitch monitor?

Are you using only cisatracurium and ateacurium? For these long cases, do you skip residing your neuromuscular blocker for a couple hours??

You can pretty reliably clinically assess a patient as reversible, mainly from the beginnings of respiratory efforts, but don't say that to an oral board examiner.

Most developing world places I've been are very stingy with NMBDs for cost reasons. Not just the cost of the NMBD, but the reversal agents too. They'd often just tolerate some residual weakness after extubation, and if the patient looked floppy give some reversal. They do a lot of small things to save money or supplies, accepting incrementally higher risk, that would freak Americans straight the hell out.

Also, did you mean to imply that cisatracurium and atracurium don't need to be reversed (untrue), or did you just mean they're more predictable in duration that rocuronium or vecuronium (true)?
 
You can pretty reliably clinically assess a patient as reversible, mainly from the beginnings of respiratory efforts, but don't say that to an oral board examiner.

Most developing world places I've been are very stingy with NMBDs for cost reasons. Not just the cost of the NMBD, but the reversal agents too. They'd often just tolerate some residual weakness after extubation, and if the patient looked floppy give some reversal. They do a lot of small things to save money or supplies, accepting incrementally higher risk, that would freak Americans straight the hell out.

Also, did you mean to imply that cisatracurium and atracurium don't need to be reversed (untrue), or did you just mean they're more predictable in duration that rocuronium or vecuronium (true)?
Much more reliable, and both shorter acting. I often feel rocuronium is so variable that I would feel uncomfortable not reversing someone if I had redosed it at some point.
 
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