laryngospams and propofol

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epidural man

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I've always imagined that laryngospasm was a stage II phenomenon.

I had a pediatric anesthesiologist tell me years ago that patients on just propofol (with no volatile anesthetic) will not go into laryngospasm while under the influence of propofol (because there are not stages with propofol anesthetic, just different depths).

What say you all? Can you have laryngospasm under a propofol infusion? If you do think that, why? Also, can you support this claim with the written word?
 
I've always imagined that laryngospasm was a stage II phenomenon.

I had a pediatric anesthesiologist tell me years ago that patients on just propofol (with no volatile anesthetic) will not go into laryngospasm while under the influence of propofol (because there are not stages with propofol anesthetic, just different depths).

What say you all? Can you have laryngospasm under a propofol infusion? If you do think that, why? Also, can you support this claim with the written word?

Yes you can..

A propofol drip provides depth of anesthesia through the stages like anything else. I think the descent and ascent is just faster, but you can certainly put a kid "inbetween" in the "stage 2" zone and have a laryngospasm due to airway secretions for example..

You have a young and vital 12 yo kid who is "inbetween" at say 50-125 mcg/kg/min of prop for endoscopy for example when saliva or scope hits the cords

You can even have laryngospasm outside of stage 2 well into GA under the right conditions
 
I agree completely with @Hoya11 . The stages are just faster especially with an induction dose bolus. But, on a drip or titrating small bonuses can 100% put you in that tweener hyperexcitable stage. Like the pt with an SAB on a gtt for a TKA that starts coughing uncontrollably, or the guy waking up from his EGD that starts going wild, or the pt that wasn’t quite ready for the LMA that bites and breath holds, etc.

Sorry no literature, just stool time to back it up.

And L-spasm is certainly not solely a stage 2 phenomenon. I know somebody that spasmed wide awake at home when he had bronchitis. Scared the crap outta him. It’s also a natural phenomenon that occurs when liquids or foreign bodies hit the larynx, and is often considered a component of the mammalian dive reflex.
 
No argument with any of the above...but...never, not once (>20 yrs, lots of peds) have I had to mangage a larygospasm while using propofol in any delivery system.

BTW, we call it "bag time" in these parts :naughty:
 
I “feel” like (not scientific at all) patients go through obvious stages when you are inducing anesthesia with propofol. Normally we slam in a syringe or two and give paralytic, so we don’t notice it. However, when you slowly titrate propofol, you definitely see stages. However, when a patient is emerging from a propofol anesthetic, I rarely see the stages that occur when emerging from a volatile anesthetic. A 20 year old dude emerging from a volatile anesthetic and I have my boxing gloves on, but that same 20 year old dude will likely wake up like a church mouse from a propofol anesthetic. I often wake young guys up with propofol for this very reason.
 
I've always imagined that laryngospasm was a stage II phenomenon.

I had a pediatric anesthesiologist tell me years ago that patients on just propofol (with no volatile anesthetic) will not go into laryngospasm while under the influence of propofol (because there are not stages with propofol anesthetic, just different depths).

What say you all? Can you have laryngospasm under a propofol infusion? If you do think that, why? Also, can you support this claim with the written word?
I side with the anesthesiologists who told you that. Are you sure it wasn't me?

Thinking about Stage 2 with propofol is silly and shows one dimensional thought process.

That being said anyone can laryngospasm at any random time with the proper stimulus, not related to being in "stage 2".
 
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Most of the Society for Pediatric Sedation (so the data set is almost entirely outside the OR) data would suggest the laryngospasm rate for kids and propofol if less than 0.5% but definitely a risk. You can find nicely categorized links on the SPS website (pedsedation.org)

As someone who contributes to the database, the caveat is that you're relying on providers classifications from many, many sites and so the definition for laryngospasm may not be quite as defined as it would be for y'all. Not saying it's not accurate, just that things might be oversimplified in one direction or the other.
 
I agree completely with @Hoya11 . The stages are just faster especially with an induction dose bolus. But, on a drip or titrating small bonuses can 100% put you in that tweener hyperexcitable stage. Like the pt with an SAB on a gtt for a TKA that starts coughing uncontrollably, or the guy waking up from his EGD that starts going wild, or the pt that wasn’t quite ready for the LMA that bites and breath holds, etc.

Sorry no literature, just stool time to back it up.

And L-spasm is certainly not solely a stage 2 phenomenon. I know somebody that spasmed wide awake at home when he had bronchitis. Scared the crap outta him. It’s also a natural phenomenon that occurs when liquids or foreign bodies hit the larynx, and is often considered a component of the mammalian dive reflex.

True story;

15 years ago I was kayaking on a dam-released river with VERY cold water. I had a cold/cough at the time. Great idea right? Breathed in a splash of ice water and bam! Larnygospasm. Lasted maybe 6-8 seconds but I thought it was the end. Terrifying.
 
True story;

15 years ago I was kayaking on a dam-released river with VERY cold water. I had a cold/cough at the time. Great idea right? Breathed in a splash of ice water and bam! Larnygospasm. Lasted maybe 6-8 seconds but I thought it was the end. Terrifying.

Did you Larson maneuver yourself?
 
I've always imagined that laryngospasm was a stage II phenomenon.

So-called "chest wall rigidity" from opiates has been nicely shown to be vocal cord closure, so there's at least one other not-rare and not-stage-2 cause of laryngospasm.
 
So-called "chest wall rigidity" from opiates has been nicely shown to be vocal cord closure, so there's at least one other not-rare and not-stage-2 cause of laryngospasm.
You can still have chest wall rigidity in an intubated patient so its not always entirely due to vocal cord closure.
 
You can still have chest wall rigidity in an intubated patient so its not always entirely due to vocal cord closure.

Chest wall rigidity from what? Narcotic? Not bloody likely. More likely from lack of paralysis.
 
You can still have chest wall rigidity in an intubated patient so its not always entirely due to vocal cord closure.
🙂

Whether the quantity of angels dancing on that pin is 1 or 2, the point was that laryngospasm can occur in the absence of volatile anesthetics and the classic stage 2 hyperexcitable state.
 
🙂

Whether the quantity of angels dancing on that pin is 1 or 2, the point was that laryngospasm can occur in the absence of volatile anesthetics and the classic stage 2 hyperexcitable state.
Yes and it was a good point
 
Ask Joan Rivers
Stole my line....glad I read the comments before commenting myself. I think time in endoscopy will convince you that it is possible with propofol albeit less common.

Has anyone tried breaking a laryngospasm with propofol instead of succinylcholine? I will consider it for the next one I have. But if I really have a situation that needs sux, I am not going to experiment with propofol.
 
Intubation with prop/remi. Chest wall rigidity with poor compliance with marked improvement after allowing the remi to wear off. Ive also given sux in that same situation.
So do you associate poor pulmonary compliance with chest wall rigidity or did you have difficulty with mask ventilation?
I love to intubate with remi, i do it often and i have never ever had any compliance problem.
 
So do you associate poor pulmonary compliance with chest wall rigidity or did you have difficulty with mask ventilation?
I love to intubate with remi, i do it often and i have never ever had any compliance problem.
In the case I mentioned chest wall rigidity. I have also seen vocal cord closure due to remi with difficulty mask ventilating.
 
Stole my line....glad I read the comments before commenting myself. I think time in endoscopy will convince you that it is possible with propofol albeit less common.

Has anyone tried breaking a laryngospasm with propofol instead of succinylcholine? I will consider it for the next one I have. But if I really have a situation that needs sux, I am not going to experiment with propofol.

Yes u can break spasm with propofol or whatever else that rapidly deepens the anesthetic. I do jaw thrust, PPV, then propofol, then if all else fails 0.1-0.2 mg/kg suxx
 
As others have said, laryngospasm most definitely occurs with propofol. We do alot of peds ENT airway evals with rigid bronchs at my shop on propofol gtt alone in kids. It is fairly common when ENT first takes a look with their rigid scope that the kids spasm down and you see it on the nice TV screen. 0.5-1mg/kg of propofol later everything is perfect.
 
As others have said, laryngospasm most definitely occurs with propofol. We do alot of peds ENT airway evals with rigid bronchs at my shop on propofol gtt alone in kids. It is fairly common when ENT first takes a look with their rigid scope that the kids spasm down and you see it on the nice TV screen. 0.5-1mg/kg of propofol later everything is perfect.
Is that really a spasm or the cords doing what they are supposed to on a patient not properly anesthetized for the stimulus they are receiving?

I would say it is the latter.
 
High dose opioids absolutely can cause involuntary muscle contraction. Happens at the chest wall, the cords, everywhere. If you haven't seen it, you just haven't given enough opioid. We have talked about this multiple times in the past.

In residency, we were trained to do cranis with high dose opioid titration to the edge of apnea, then induce. I'm talking typically 750-1250mcg fent with nothing else on board. Probably 20% of the time, the pt would get rigid, and I'm talking involuntary contraction of arms, legs, you name it. Almost decorticate type posturing. Nothing a little prop/roc doesn't fix, but it is a very real/reproducible phenomenon.
 
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It's the same thing. The vocal cords slamming shut is a spasm.

By your definition you have a laryngospasm every time you swallow. Food, liquid, saliva... you have thousands of spasms a day.
 
In residency, we were trained to do cranis with high dose opioid titration to the edge of apnea, then induce. I'm talking typically 750-1250mcg fent with nothing else on board. Probably 20% of the time, the pt would get rigid, and I'm talking involuntary contraction of arms, legs, you name it. Almost decorticate type posturing. Nothing a little prop/roc doesn't fix, but it is a very real/reproducible phenomenon.

Why would anyone think that is a good way to induce for any case, let alone cranis?
 
I never realized Salty dog was a girl.

Should be Salty b....h properly speaking.

Dude, @urge fellin' feisty on a Friday morning. Take it easy bud. And I think you missed the double entendre @ZzzPlz was making.

Like @eikenhein said, closing is not the same as spasm. Just like flexing my hamstring is not the same as a charlie horse.

Why would anyone think that is a good way to induce for any case, let alone cranis?

It's an absolutlely beautiful anesthetic for a crani. There's more to it than just the upfront fentanyl load, but patients wake up buttery smooth and clear headed. This is the technique of choice for the guys that wrote the euro chapters in Miller. They are excellent clinicians - not just academics.

Now go smoke a beer and drink a fatty and chill out man.
 
So do you associate poor pulmonary compliance with chest wall rigidity or did you have difficulty with mask ventilation?
I love to intubate with remi, i do it often and i have never ever had any compliance problem.

How much remi are u giving? The studies I find quote 4-5mcg/kg to obtain ideal intubating conditions and I never seen people give such a large bolus where I am.
 
High dose opioids absolutely can cause involuntary muscle contraction. Happens at the chest wall, the cords, everywhere. If you haven't seen it, you just haven't given enough opioid. We have talked about this multiple times in the past.

In residency, we were trained to do cranis with high dose opioid titration to the edge of apnea, then induce. I'm talking typically 750-1250mcg fent with nothing else on board. Probably 20% of the time, the pt would get rigid, and I'm talking involuntary contraction of arms, legs, you name it. Almost decorticate type posturing. Nothing a little prop/roc doesn't fix, but it is a very real/reproducible phenomenon.

Perhaps versed makes a big difference...I give fentanyl by the fluid ounce (or the equivalent sufenta) and just have not had a patient do that, much less 20 % of them. Nor do my peers...I asked.
 
That's what i give

Assume 70kg patient x 5mcg/kg remi = 350mcg x 25mcg/ml = 14cc remi.

I have never bolused more than a 100mcg remi before! Are you pretreating with glyco, pressors? Any bad hemodynamic SEs? How much propofol are you giving? Does the patient relax the jaw and vocal cords same as giving paralytic?

I'm excited to try this but I know my attendings will not let me give that large a remi bonus :/
 
Assume 70kg patient x 5mcg/kg remi = 350mcg x 25mcg/ml = 14cc remi.

I have never bolused more than a 100mcg remi before! Are you pretreating with glyco, pressors? Any bad hemodynamic SEs? How much propofol are you giving? Does the patient relax the jaw and vocal cords same as giving paralytic?

I'm excited to try this but I know my attendings will not let me give that large a remi bonus :/

A) Just dont dilute it so much

B) Remi is equipotent to fentanyl. That’s not really that big of a dose.

Alfentanil also works really well in lieu of paralytic.
 
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I dilute 2mg in 5cc and give 1cc more or less 😉
You typically see tachycardia upon induction, the patient might cough due to vocal cord closure 😉 ,then when the HR slows down you know the remi is kicking in and it's time to intubate.

I probably give a little less propofol than for a normal patient but not much.
Never had an adverse reaction apart from hypotension if the patient is not a ypung asa1
 
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It's an absolutlely beautiful anesthetic for a crani. There's more to it than just the upfront fentanyl load, but patients wake up buttery smooth and clear headed. This is the technique of choice for the guys that wrote the euro chapters in Miller. They are excellent clinicians - not just academics.

Now go smoke a beer and drink a fatty and chill out man.

How bad is the patients bp sagging after pinning is done and the case begins? Every time I've tried to futz around with high dose fent I've had to run stupid amounts of neo for the next two hours because the crani itself isn't that stimulating and the sympathetics are completely abolished after a mg of fent. In my experience, high dose prop bolus (dec cmro2, cbf) +- vasopressor bolus is a much more elegant and shorter acting method, plus the pt still wakes up beautifully if you emerge on a low dose prop gtt.
 
How much remi are u giving? The studies I find quote 4-5mcg/kg to obtain ideal intubating conditions and I never seen people give such a large bolus where I am.
I think 4-5ug/kg is too much. 2-3ug/kg is quite effective with less side effects
 
A) Just dont dilute it so much

B) Remi is equipotent to fentanyl. That’s not really that big of a dose.

Alfentanil also works really well in lieu of paralytic.
Remi is at least twice as potent as fentanyl. Thats a big dose
 
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