#Case_03 Sux apnea sucks, but was it Sux?

[DrAmir0078]

Young age male, 85 kg had a PNL procedure and was paralyzed with rocuronium (all other premed, induction, maintenance as usual), his Op lasts two hours, reversal of NMB was done with neostigmine and atropine.
Anyway, after almost two hours, after discharge, we needed to Op him for another procedure for less than 20 minutes.
We gave him Propofol 250 mg and wasn't successful, Sux was addressed, we gave him 50 mg only. Procedure was successful.
Patient was kept on bag mask ventilation for 30 minutes, during these 30 minutes, only nasal flaring was noticed (no TOF as you know), then with continued BMV, his blood pressure peaked up, marked sweating, we suspected Scoline Apnea, we ordered blood, tubed him (was very easy), kept on ventilation, his blood pressure reached 200/90, sweating continued.
Blood arrived (wasn't fresh) - once we gave 20 ml, patient gains noticeable improvement and power, we gave him incremental 20 ml of blood and almost 300 ml were given and the patient woke up completely (it took two hours after sux), extubation done, his VS return normal.
We gave his relatives a paper written on it "scoline apnea risk"

What do you think?

Was it Sux apnea?

Or prior neostigmine effects of reversal prolonged Sux? It was only 50 mg!

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[vector2]

My bet is the neostigmine caused it rather than the pt having congenital pseudocholinesterase deficiency. It's known that administering sux within a couple hours of neostigmine can lead to a prolonged block, partly because neostigmine administration also decreases pseudocholinesterase activity. Remember that the ED95 for sux is less than 0.3 mg/kg, so 50 mg is still a significant dose. Also, your patient had classic signs of inadequate neuromuscular blockade reversal- you must provide sedation and/or amnestics when you suspect this to be the case, especially in a young pt who is likely to remember the whole event.

Additionally, were you giving whole blood? We typically administer nothing for PCD (other than sedation, mechanical ventilation and time) but if it had to be treated I would administer FFP.

 

[DrAmir0078]

My bet is the neostigmine caused it rather than the pt having congenital pseudocholinesterase deficiency. It's known that administering sux within a couple hours of neostigmine can lead to a prolonged block, partly because neostigmine administration also decreases pseudocholinesterase activity. Remember that the ED95 for sux is less than 0.3 mg/kg, so 50 mg is still a significant dose. Also, your patient had classic signs of inadequate neuromuscular blockade reversal- you must provide sedation and/or amnestics when you suspect this to be the case, especially in a young pt who is likely to remember the whole event.

Additionally, were you giving whole blood? We typically administer nothing for PCD (other than sedation, mechanical ventilation and time) but if it had to be treated I would administer FFP.

Reading through, what made you think he had inadequate NMB reversal?
Good point to remember about ED95 of succinylcholine!

Yes, it was whole blood (was prepared prior to PNL), but here they cross match as usual and wasn't from his family.

We thought of giving nothing rather than wait and give sedation, but waiting on the feasibility of finding a vacant bed at our ICU/RCU (was full) over the time in the OR, made us go on plan B by administrating whole blood, and we didn't want to administer FFP because of the storage might affect the PCE!

Thanks Vector2

 

[vector2]

Reading through, what made you think he had inadequate NMB reversal?
Good point to remember about ED95 of succinylcholine!

Yes, it was whole blood (was prepared prior to PNL), but here they cross match as usual and wasn't from his family.

We thought of giving nothing rather than wait and give sedation, but waiting on the feasibility of finding a vacant bed at our ICU/RCU (was full) over the time in the OR, made us go on plan B by administrating whole blood, and we didn't want to administer FFP because of the storage might affect the PCE!

Thanks Vector2

Tachycardia, hypertension, diaphoresis, and nasal flaring are classic signs of being awake while still being paralyzed.

 

[DrAmir0078]

Tachycardia, hypertension, diaphoresis, and nasal flaring are classic signs of being awake while still being paralyzed.

Yes, indeed - definitely we thought of it, but "reversal word", now I am aware of your question. That will make neostigmine is the cause, rather than PCD, isn't it?
Because if it was CPED, we normally won't get twitching vs nasal flaring that fast! So it was inadequate NMB reversal - the reversal here is the metabolism of succinylcholine with PSE that was very short because of prior effects of neostigmine.
Very interesting!

 

[DrAmir0078]

@vector2
I was discussing this case again and what we discovered, it wasn't almost two hours between the first op and the second one, it was over 3 1/2 hours.
So will that change your bet?

 

[AdmiralChz]

I am confused... did you not have a twitch monitor available? 250 of propofol was unsuccessful for... what? Then you used 50 mg of Sux, and the patient was paralyzed for > 1 hour?

 

[DrAmir0078]

I am confused... did you not have a twitch monitor available? 250 of propofol was unsuccessful for... what? Then you used 50 mg of Sux, and the patient was paralyzed for > 1 hour?

Brings confusion but speaks reality!

No twitch monitor, but I have mentioned, he got some nasal flaring/twitching after 10 minutes, with very shallow breath but otherwise completely paralyzed!