Question For Venty And Other Resident Studs

[jetproppilot]

The minutia of anesthesia is a little cob-webby in my brain so I'll ask you studs studying for your boards, since its the time when you know the most about the book-stuff of anesthesia.

Had an adult tonsil today. Surgeon takes about thirty minutes. Cisatracurium used for induction. Patient reversed at end with full dose of neostigmine/glyco. Extubated, doing fine. I had to run to start a thoracotomy. CRNA transports to PACU.

Pt laryngospasms in PACU. I'm stuck in the thoracotomy, one of my colleagues is already in the PACU when incident happens. Colleague thought she was gonna have to reintubate so gives a full sux dose. Reintubates. (I wouldve given 10-20 mg sux to break the spasm, and masked until the small dose wore off.)

Pt on vent for 2 hours. Colleague said pt had phase 2 block. Fade on TOF.
I said wasnt really a phase 2 block but rather an expected sequelae of giving a big sux dose after a full reversal for a non-depolarizer.

A friendly discussion ensued.

SOOOOOOOOOO, resident studs, is this called a phase 2 block or not?

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[DrDre']

I believe phase 2 block only occurs after relative overdosage with sux, 2nd dose etc. I believe u r correct and this is the expected consequence of giving sux after reversal agent. Becuz of the additional ach at the NMJ, the sux "lasts longer" becuz of achase having to also break down the additional ACH.

Off to the swap meet, gonna get my newly tuned skis. IF they gaffle me, I'm gonna go new orleans on their asz.

JPP, glad u r stickin around despite all the bullshiiiit on this site. dre'

The minutia of anesthesia is a little cob-webby in my brain so I'll ask you studs studying for your boards, since its the time when you know the most about the book-stuff of anesthesia.

Had an adult tonsil today. Surgeon takes about thirty minutes. Cisatracurium used for induction. Patient reversed at end with full dose of neostigmine/glyco. Extubated, doing fine. I had to run to start a thoracotomy. CRNA transports to PACU.

Pt laryngospasms in PACU. I'm stuck in the thoracotomy, one of my colleagues is already in the PACU when incident happens. Colleague thought she was gonna have to reintubate so gives a full sux dose. Reintubates. (I wouldve given 10-20 mg sux to break the spasm, and masked until the small dose wore off.)

Pt on vent for 2 hours. Colleague said pt had phase 2 block. Fade on TOF.
I said wasnt really a phase 2 block but rather an expected sequelae of giving a big sux dose after a full reversal for a non-depolarizer.

A friendly discussion ensued.

SOOOOOOOOOO, resident studs, is this called a phase 2 block or not?

 

[bubalus]

If I remember correctly, one of the other issues you face here is that the neostigmine does a great job of inhibiting pseudocholinesterase, so the net result is as if you gave sux to someone with atypical pseudocholinesterase, hence the prolonged block.

Miller says, "Phase II block is a complex phenomenon that occurs slowly at junctions continuously exposed to depolarizing agents. The junction is depolarized by the initial application of a depolarizing relaxant, but then the membrane potential gradually recovers toward normal, even though the junction is still exposed to drug. Neuromuscular transmission usually remains blocked throughout the exposure. Several factors are involved. The repeated opening of channels allows a continuous efflux of potassium and influx of sodium, and the resulting abnormal electrolyte balance distorts the function of the junctional membrane. Calcium entering the muscle through the opened channels can cause disruption of receptors and sub-end-plate elements themselves. The activity of a sodium-potassium adenosine triphosphatase pump in the membrane increases with increasing intracellular sodium and, by pumping sodium out of the cell and potassium into it, works to restore the ionic balance and membrane potential toward normal. As long as the depolarizing drug is present, the receptor channels remain open, and ion flux through them remains high.59

Factors influencing the development phase II block include the duration of exposure to the drug, the particular drug used and its concentration, and even the type of muscle (i.e., fast or slow). Interactions with anesthetics and other agents also affect the process. All of these drugs may also have prejunctional effects on the rate and amount of transmitter release and mobilization. With so many variables involved in the interference with neuromuscular transmission, phase II block is a complex and ever-changing phenomenon. The reversal response of a phase II block produced by a depolarizing muscle relaxant to administration of cholinesterase inhibitors is difficult to predict. It is therefore best that reversal by cholinesterase inhibitors is not attempted, although the response to tetanus or train-of-four stimulation resembles that produced by nondepolarizers. "

Since you've inhibited pseudocholinesterase with the neostigmine, the NMJ is
"continuously exposed to depolarizing agents," and you've got yourself a phase II block, as evidenced by fade on TOF.

Great teaching moment. After a reversal, don't give a full dose of sux or you're going to need a vent (or be bagging for a long time).

 

[jetproppilot]

I believe phase 2 block only occurs after relative overdosage with sux, 2nd dose etc. I believe u r correct and this is the expected consequence of giving sux after reversal agent. Becuz of the additional ach at the NMJ, the sux "lasts longer" becuz of achase having to also break down the additional ACH.

Off to the swap meet, gonna get my newly tuned skis. IF they gaffle me, I'm gonna go new orleans on their asz.

JPP, glad u r stickin around despite all the bullshiiiit on this site. dre'

Preciate the shout out, Dre.

Interactions with studs like you, Venty, Noy, Zippie, UT, Mil (r.i.p.) et al are why my time here is relevant.

All the political/administrative bullsheahht is tolerated because of same.

 

[UTSouthwestern]

A small dose of propofol with lidocaine (30-50 mg propofol, 100 mg lido) will also break the spasm without prolonged effects.

 

[CremeSickle]

Really?

I tried prop. on a couple of spasms without success. Id say if they were "sick" then go suxx but if they are still maintaining a sat try prop. first. That make sense?

As for phase 2 block, it is my understanding that it can happen with either a massive dose of Sux or a repeat dose of Sux. Cholinesterase inhibitors will sometimes partially reverse phase II block. There has been some research on this which seems to suggest it does happen but not reliably.

In order to know if u have phase 2 just pop on the stimulator and look for fade in your TOF. + fade = phase 2, no fade = phase 1.

 

[fval28]

The minutia of anesthesia is a little cob-webby in my brain so I'll ask you studs studying for your boards, since its the time when you know the most about the book-stuff of anesthesia.

Had an adult tonsil today. Surgeon takes about thirty minutes. Cisatracurium used for induction. Patient reversed at end with full dose of neostigmine/glyco. Extubated, doing fine. I had to run to start a thoracotomy. CRNA transports to PACU.

Pt laryngospasms in PACU. I'm stuck in the thoracotomy, one of my colleagues is already in the PACU when incident happens. Colleague thought she was gonna have to reintubate so gives a full sux dose. Reintubates. (I wouldve given 10-20 mg sux to break the spasm, and masked until the small dose wore off.)

Pt on vent for 2 hours. Colleague said pt had phase 2 block. Fade on TOF.
I said wasnt really a phase 2 block but rather an expected sequelae of giving a big sux dose after a full reversal for a non-depolarizer.

A friendly discussion ensued.

SOOOOOOOOOO, resident studs, is this called a phase 2 block or not?

Phase 2 sounds right-
couple questions tho'-

was pt tubed on sux initially?

How much sux was given for reintubation?

Reason I ask is could this be a PSch deficiency (heterozygous atypical)?

Also seems pt may have been extubated a bit early if he laryngospasm'd in PACU.

I have seen prolonged phase I block with LARGE doses of sux (200+ mg). Although fade on TOF seems to rule this out...

My guess is Phase 2 following sux admin in the presence of incomplete nondepolarizer reversal.

 

[timtye78]

As my understanding goes, Baby Miller states to obtain Phase II block with sux you have to give 3-5 mg/kg or it may be associated with sux infusions. Which is quite a bit more than the 'normal' intubating dose of 1-2 mg/kg. I would agree with either prolongation of effect secondary to the neostigmine as most likely, then atypical cholinesterase. Other concern might be did the patient have severe liver disease?

 

[jetproppilot]

Phase 2 sounds right-
couple questions tho'-

was pt tubed on sux initially?

How much sux was given for reintubation?

Reason I ask is could this be a PSch deficiency (heterozygous atypical)?

Also seems pt may have been extubated a bit early if he laryngospasm'd in PACU.

I have seen prolonged phase I block with LARGE doses of sux (200+ mg). Although fade on TOF seems to rule this out...

My guess is Phase 2 following sux admin in the presence of incomplete nondepolarizer reversal.

Tubed on nimbex initially.

Certainly could be PSch def.

Dont know exact dose but I'm sure she gave around 140mg.

 

[jetproppilot]

As my understanding goes, Baby Miller states to obtain Phase II block with sux you have to give 3-5 mg/kg or it may be associated with sux infusions. Which is quite a bit more than the 'normal' intubating dose of 1-2 mg/kg. I would agree with either prolongation of effect secondary to the neostigmine as most likely, then atypical cholinesterase. Other concern might be did the patient have severe liver disease?

Healthy normal 20 something girl. ASA 1.

 

[bubalus]

Although she may have atypical psudocholinesterase, her pseudocholinesterase was inhibited by the neostigmine she was given, so in essence, she's functionally atypical due to the neostigmine. Whether this is sufficient to cause such a prolonged block of whether she has underlying atypical pseudocholinesterase is anyone's guess, but here's an abstract somewhat related.

Effects of Neostigmine and Pyridostigmine on Duration of Succinylcholine Action and Pseudocholinesterase Activity.

Article

Anesthesiology. 49(3):188-191, September 1978.
Sunew, Kenneth Y. M.D. *; Hicks, Robert G. M.D. +
Abstract:
Effects of the anticholinesterase drugs on the duration of action of succinylcholine (SCh) and pseudocholinesterase activity were studied in 16 adult patients undergoing general anesthesia. Each patient received two doses of SCh, 1 mg/kg, intravenously: the first dose was given before and the second dose, 5 min after neostigmine, 5 mg, or pyridostigmine, 25 mg. Electromyographic determinations were used to measure the duration of SCh-induced block. Prolongation in the neostigmine group (n = 8) was compared with that in the pyridostigmine group (n = 8). Pseudocholinesterase activities were determined before, during, and at the point of full recovery of neuromuscular blockade by the second dose of SCh.

The effect of SCh, 1 mg/kg, was significantly prolonged from the control value, 11.1 +/- 1.43 (mean +/- SE), to 35 +/- 3.24 min following neostigmine, and from 13.1 +/- 1.45 to 23.9 +/- 2.5 min after pyridostigmine. Pseudocholinesterase activities determined 5 min after administration of neostigmine and pyridostigmine were decreased to 21 and 20 per cent of control, respectively. Full recovery from the SCh-induced block was observed, while enzymatic activities remained suppressed to 47 and 39 per cent of control in the neostigmine and pyridostigmine groups, respectively. The neuromuscular blocking effect of SCh was significantly prolonged by both neostigmine and pyridostigmine, but more by neostigmine. It is concluded that the enzyme may not be the sole factor determining the effect of anticholinesterase drugs on the duration of action of SCh.

 

[VentdependenT]

Based on the TOF and Tetany FADE its a phase II.

Cause is the obliteration of the pseudocholinesterase function by Neostigmine. You can't eliminate the sux, so it hangs around, causes your phase II block.

UT/Jet, I've only had one severe laryngospasm in an adult and I pushed 1mg/kg of sux. I didn't wanna F around. Sats already heading in the toilet.

If its a "little" laryngospasm (stridor but still moving air) you think 20mg of Propofol + some Pos Press is better than just Pos Press alone?

Sux is so friggen reliable.

 

[thegasman]

sounds like a phase II block - secondary to inhibition of pseudocholinesterase by neostigmine. I wonder if 10-20 mg of succ would have broken the laryngospasm without prolonged blockade?

 

[leaverus]

I'm confused. What's the difference between calling it phase II block and "an expected sequelae of giving a big sux dose after a full reversal for a non-depolarizer."? It appears to me to be the same thing in this situation.

 

[ear-ache]

A little off topic but...

Has anyone had experience with using the "laryngospasm notch" to break laryngospasm?

It is described by Dr. Philip in the 3rd edition of Morgan & Mikhail, as well as;
http://www.anesthesiology.org/pt/re...MzBSKNL1MjsshGBb!1899110359!181195628!8091!-1

Thanks,
e

 

[UTSouthwestern]

A little off topic but...

Has anyone had experience with using the "laryngospasm notch" to break laryngospasm?

It is described by Dr. Philip in the 3rd edition of Morgan & Mikhail, as well as;
http://www.anesthesiology.org/pt/re...MzBSKNL1MjsshGBb!1899110359!181195628!8091!-1

Thanks,
e

Yes. It seems to work, but would be hard to defend that you chose that course of action instead of something more definitive as the patient is desaturating.

I use it as part of my jaw thrust technique with an otherwise unoccupied finger performing the pressure as the rest are performing the jaw thrust.

 

[UTSouthwestern]

Really?

I tried prop. on a couple of spasms without success. Id say if they were "sick" then go suxx but if they are still maintaining a sat try prop. first. That make sense?

It isn't instantaneous. A good 30-60 seconds, but it has worked for me several times, especially with the lidocaine.

 

[VentdependenT]

Yes. It seems to work, but would be hard to defend that you chose that course of action instead of something more definitive as the patient is desaturating.

I use it as part of my jaw thrust technique with an otherwise unoccupied finger performing the pressure as the rest are performing the jaw thrust.

It works. You gotta really dig in though and hold. Very hard to do if your also trying to hold Pos Press with a mask. Good to have a extra hand around then.

 

[dhb]

Pt on vent for 2 hours.

Correlates well with the duration of action of neostigmine so it wouldn't bet on pseudocholinesterase deficiency even if it could theoretically be a cause
good teaching point

 

[jetproppilot]

The minutia of anesthesia is a little cob-webby in my brain so I'll ask you studs studying for your boards, since its the time when you know the most about the book-stuff of anesthesia.

Had an adult tonsil today. Surgeon takes about thirty minutes. Cisatracurium used for induction. Patient reversed at end with full dose of neostigmine/glyco. Extubated, doing fine. I had to run to start a thoracotomy. CRNA transports to PACU.

Pt laryngospasms in PACU. I'm stuck in the thoracotomy, one of my colleagues is already in the PACU when incident happens. Colleague thought she was gonna have to reintubate so gives a full sux dose. Reintubates. (I wouldve given 10-20 mg sux to break the spasm, and masked until the small dose wore off.)

Pt on vent for 2 hours. Colleague said pt had phase 2 block. Fade on TOF.
I said wasnt really a phase 2 block but rather an expected sequelae of giving a big sux dose after a full reversal for a non-depolarizer.

A friendly discussion ensued.

SOOOOOOOOOO, resident studs, is this called a phase 2 block or not?

Thanks for all your great responses! Ya'll some smart mo foes.

 

[Lonestar]

140 mg of succ? thats a lot of succ for a "healthy" 20 yr old. I have had some spasms in the pacu, but none that required that much succ. looks like a expected response to giving that much succ. pt recently had neostigmine (increases Ach and ineffective pseudocholinesterase + "strong" dose of succ = weak pt for long time).

 

[jetproppilot]

140 mg of succ? thats a lot of succ for a "healthy" 20 yr old. I have had some spasms in the pacu, but none that required that much succ. looks like a expected response to giving that much succ. pt recently had neostigmine (increases Ach and ineffective pseudocholinesterase + "strong" dose of succ = weak pt for long time).

I agree.

 

[atrxnasd]

Really?

I tried prop. on a couple of spasms without success. Id say if they were "sick" then go suxx but if they are still maintaining a sat try prop. first. That make sense?

As for phase 2 block, it is my understanding that it can happen with either a massive dose of Sux or a repeat dose of Sux. Cholinesterase inhibitors will sometimes partially reverse phase II block. There has been some research on this which seems to suggest it does happen but not reliably.

In order to know if u have phase 2 just pop on the stimulator and look for fade in your TOF. + fade = phase 2, no fade = phase 1.

Of course in this case right after the Sux there would be no twitch. Prop and versed often work for paradoxical vocal cord movement. I assume other efforts were made to ventilate before the sux was given. The dose of sux is usually proportion to the amount of panic the one administering the sux is in.