is it bad to give Nondepolarizing muscle relaxant after reversal?

[IFNgamma]

ok, I tried to find the answer to this on Miller and Barash but can't find anything, perhaps some of you can help.

So I did this thryroidectomy case, case went fine, surgeons closed, pt extuabated. Then they noticed a hematoma so we had to re-intubate so they can fix it.

So I gave some roc after the re-intubation. One of the attendings that came to help out said that was a big "no-no" and said you should not give any non-depolarizing drugs after giving the reversal drugs. Why is that? He pretty much called me an idiot for not knowing that and made it seem like it should be obvious to anyone. What the hell?

As I understand it, neostigmine lasts an hr so it would have an antagonizing effect on the roc, so more roc may be required for paralysis. What is so bad about what I did? Am I missing something? Like would it cause a phase 2 block or something? Now this attending is known for being difficult, especially to CA-1s, so it could be he was taking yet another opportunity to put me down.

This is the first time I had to deal w/ a scenario that required re-intubation soon after extubation in the OR so I don't have any experience in this at all. Anyone have any ideas?

Thank you!

frustrated CA-1.

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[Planktonmd]

There is no problem in giving a non depolarizing muscle relaxant to intubate after reversal.
It might take a little bit longer to work and you might need more medicine but there is no problem other than that.
Your attending is obviously a typical academia guy who feels that he needs to dramatize everything and transform silly irrelevant issues into major events so he could appear important.

 

[Jeff05]

i agree. no issue.
may he meant that you shouldn't give a DEpolarizing relaxant (sux) after reversal, which would prolong it's duration 2/2 pseudocholinesterase inhibition.

 

[Dejavu]

I remember back when all I had was pancuronium and had to reverse it, give more when the surgeon re-opened, reversed that, then had to give another dose when they re-opened for the third time, reversed that and the patient did fine.

Put a twitch monitor on the pt and just relax. Everything will be fine. This is why God invented ventilators in the ICU.

 

[huktonfonix]

It will make the onset and duration less predicatable which is more of an annoyance than a catastrophe. like someone else said, thats why we have vents. He is right however in the fact that, yes you should have known that. At this point in CA1 year you should at least know the basics about your drugs and how they work.

 

[drmwvr]

At this point in CA1 year you should at least know the basics about your drugs and how they work.

Sounds like he did know the basics. Thats why he was confused. You sound a lot like his attending.

 

[huktonfonix]

Sounds like he did know the basics. Thats why he was confused. You sound a lot like his attending.

I think you need to reread his post. He doesnt seem to understand the basics as well as he should. I dont think his attending should have made such a big deal about it, but if you want to be good at what you do, you need to know the basics. Now, if he knew the basics he could have argued with his attending and told him "fine, the onset and duration mayl be less predictable, but given the situation I would like to optimize my intubating conditions and feel the risk of possible prolonged ventilation is outweighted by the benefit of securing the airway in a timely manner." We had a couple of those attendings back in residency, but as long as you were able to argue your point and back it up they would usually accept it even if it wasnt what they wouldve done.

 

[Consigliere]

No

 

[RussianJoo]

So what would have made the attending happy? what should you have used for the re-intubation?

 

[drmwvr]

So I gave some roc after the re-intubation. .

So, what did you use for the re-intubation?

 

[IceDoc]

i agree. no issue.
may he meant that you shouldn't give a DEpolarizing relaxant (sux) after reversal, which would prolong it's duration 2/2 pseudocholinesterase inhibition.

Just so everyone knows, this really DOES happen. It's not just one of those theoretical academic mental exercises.

(fortunately I was taking care of him a few days later, and was not the one who had to call an unplanned ICU admit. I think it was about 4hrs before he was able to be extubated).

 

[IFNgamma]

So, what did you use for the re-intubation?

nothing. The pt at that point was awake and fully reversed and he attempted to re-intubate the pt but couldn't do it even though went I intubated her it was super easy. This wasn't even his case, he just came in and went for the DL and forbid any drugs to be given.

Then my real attending came in and asked for a bit of Succ and intubated successfully. He was a little ticked later when he found out attending #1 didn't give anything before attempting to do DL. Good thing the pt did not remember the 2nd intubation at all.

 

[urge]

is it bad to give Nondepolarizing muscle relaxant after reversal?

No. You just need 4 twitches/tetanus before extubating without giving a toxic dose of neostigmine. You might have to wait, but there is nothing inherently wrong with it.

Sounds like you attending is a douche. Stay away from him/her.

BTW, I hate muscle relaxants. Nothing wrong with the drug. It's the people using them. I have had to ambu pts in pacu for ~30 min because of idiots using muscle relaxants.

 

[SleepIsGood]

fyi you get phase 2 blocks with using a lot or repeating doses of DEpolarizing agents. You dont get phase 2 blocks with NON depols.

 

[thegasman]

Just so everyone knows, this really DOES happen. It's not just one of those theoretical academic mental exercises.

(fortunately I was taking care of him a few days later, and was not the one who had to call an unplanned ICU admit. I think it was about 4hrs before he was able to be extubated).

Sometimes you HAVE to give the sux - like in post-extubation larygospasm - I had one a couple of weeks ago - I go in at wakeup and.... patient blue, crna can't ventilate, sats read 14%. (oh the joy of crna supervision) So we gave a touch of sux and things got better real fast. But it does take longer than you think to wear off after reversal has been given (20mg took 20 min).

 

[BLADEMDA]

Acta Anaesthesiol Scand. 1995 Aug;39(6):744-7. Links

Comparison of the effects of neostigmine and edrophonium on the duration of action of suxamethonium.

McCoy EP, Mirakhur RK.
Department of Anaesthetics, Queen's University of Belfast, Northern Ireland.
Rapid sequence induction of anaesthesia necessitating the use of suxamethonium may occasionally be needed soon after antagonism of neuromuscular block with anticholinesterase agents. The onset and duration of action of 1 mg kg-1 of suxamethonium was recorded in groups of 10 patients each, 5 or 10 min after the administration of edrophonium 1 mg kg-1 or neostigmine 40 micrograms kg-1 given for the antagonism of atracurium-induced neuromuscular block. Plasma cholinesterase activity was measured before, and 5 and 10 min after the administration of the anticholinesterases. A further 10 patients received suxamethonium 1 mg kg-1 without prior atracurium or anticholinesterase administration to serve as controls. The onset of action of suxamethonium was significantly prolonged when administered 5 min after both anticholinesterases, compared to the control group (P < 0.01). Recovery of suxamethonium block was delayed significantly after neostigmine, compared to both the edrophonium and the control groups (P < 0.05-0.001). Plasma cholinesterase activity was significantly reduced with the use of neostigmine but not with edrophonium (P < 0.001).

 

[BLADEMDA]

There are case reports of the Sux taking two hours to wear off in a patient in this situation with chronic renal failure.

 

[BLADEMDA]

Let me take a stab at your orginal question on this thread.

After giving a dose of reversal agents the Rocuronium has been "competitively" antagonized at the neuromuscular junction. Some of the original rocuronium was displaced through "redistribution" (primary route for one dose) and some more was metabolized via the liver-bile (most)/kidney (less). Then, the remainder of the rocuronium is "booted off" the neuromuscular junction by the Neostigmine.

So, when you give additional Rocuronium the Neostigmine is "competitvely" displaced from the neuromuscular junction. This may make "reversing" the patient a second time more difficult in the near term.

Your attending probably prefered the SUX route if additional "short" paralysis was needed after giving reversal agents. The SUX (around 60-80 mg) should last 10-20 minutes before being dissipated from the neuromuscular junction. Plus, no additional reversal agents are needed with the SUX. Remember, by giving the Neostigmine prior to the SUX there will be a prolongation of duration of SUX induced paralysis.

 

[BLADEMDA]

Depolarization Neuromuscular Blockade

Succinylcholine (Anectine)​

• Time course:
  • rapid onset (30-60 seconds) -- IV
  • short duration of action: 3-5 minutes
• Applications
  • Skeletal muscle relaxation, facilitating intubation
• Mechanism of Action:
  • Succinylcholine (Anectine) binds to nicotinic cholinergic receptors
    • Promotes post synaptic membrane depolarization causing a relatively long-term depolarization (compared acetylcholine) due to reduced synaptic breakdown.
    • Blockade occurs because depolarized membrane is unresponsive to subsequent acetylcholine-receptor interaction
• Phases -- Phase I
  • Depolarization component is the phase I blockade
  • Prolonged phase I blockade may be associated with potassium transport (from inside cell out): which may increase serum potassium by 0.5 mEq/L.
  • Properties of phase I blockade:
    • Reduced amplitude; sustained response to continuous electrical stimulation
    • Reduced contractile-response to single twitch stimulus
    • Enhanced neuromuscular-blockade following anticholinesterase drug administration
    • Train-of-four (TOF) ratio of > 0.7 (the height of the 4th twitch to that of the 1st twitch); a measure of presynaptic membrane effects. When the single twitch height has recovered to about 100%, the train-of-four ratio is about 70%.
    • No post-tetanic facilitation
    • Skeletal muscle fasciculations are associated with initial (onset) succinylcholine (Anectine) action.
• Phases -- Phase II
  • Continued succinylcholine (Anectine) administration results in a transition from endplate depolarization to endplate repolarization.
  • However, this repolarization state is not susceptible to acetylcholine depolarization provided succinylcholine (Anectine) remains present
    • Blockade, even following repolarization, has led to the description of phase II block as "a desensitization blockade".
  • Transition from a phase I to a phase II blockade may be rapid (following a succinylcholine (Anectine) dose of 2-4 mg/kg IV)
    • Phase II onset: initial manifestation -- tachyphylaxis with need to increase succinylcholine (Anectine) infusion rate or to administer larger doses
    • Various degrees of phase I & phase II blockade may coexist
    • Mainly phase I: -- anticholinesterases enhance neuromuscular-blockade
    • Mainly phase II: --anticholinesterases antagonize phase II blockade
      • Small doses of edrophonium (Tensilon) (0.1-0.2 mg/kg, IV) may be useful in discriminating phase I vs. phase II block
• Time course/Duration of Action -- Succinylcholine (Anectine)
  • Duration of action determined by plasma cholinesterase-mediated succinylcholine (Anectine) hydrolysis
    • Plasma cholinesterase: hepatic enzyme
    • Initial succinylcholine (Anectine) metabolite: succinylmonocholine (very weak neuromuscular-blocking)
  • Plasma cholinesterase activity determines the amount of succinylcholine (Anectine) reaching the endplate {most succinylcholine (Anectine) is hydrolyzed by plasma enzyme}
  • Factors influencing plasma cholinesterase (pseudocholinesterase) activity
    • Reduced hepatic enzyme synthesis
    • The presence of atypical (genetic) plasma cholinesterase which exhibits reduced succinylcholine (Anectine) hydrolytic capacity
    • Liver disease (severe)
    • Drug effects, e.g. neostigmine (Prostigmin) -- a carbamylating cholinesterase inhibitor
• Drugs which may prolong succinylcholine (Anectine) action due to effects on pseudocholinesterase:
  • Insecticides
  • Nitrogen mustard, cyclophosphamide (Cytoxan) -- plasma cholinesterase inhibition
  • Metoclopramide (Reglan) (10 mg IV)
  • High estrogen levels (parturients)
• Resistance to succinylcholine (Anectine)
  • Genetic: increased plasma cholinesterase activity
  • Obesity -- more plasma cholinesterase activity
  • Pharmacodynamic effects, e.g. myasthenia gravis
    • In myasthenia gravis: reduced number of nicotinic, neuromuscular junctional receptors -- the target for the drug succinylcholine (Anectine)
• Atypical Pseudocholinesterase (plasma cholinesterase)
  • Consequence: prolonged neuromuscular-blockade (1-3 hours) following normal succinylcholine (Anectine) dosage
  • Dibucaine (Nupercainal, generic)-related cholinesterase variant: most important
    • Dibucaine is an amide local anesthetic that inhibits wild type plasma cholinesterase by 80%; however, it inhibits atypical enzyme by only 20%.
    • If dibucaine (Nupercainal, generic) number equals 80: normal cholinesterase
    • If dibucaine (Nupercainal, generic) number equals 20: homozygous for atypical cholinesterase -- frequency = 1/3200
• Clinical consequences of atypical cholinesterase on neuromuscular-blockade duration
  • 1 mg/kg IV succinylcholine (Anectine): > three hours duration
  • 25% recovery of single twitch response following 0.03 mg/kg IV {small dose} mivacurium (Mivacron): 80minutes
  • For heterozygous atypical plasma cholinesterase patients (frequency: 1/480) -- dibucaine (Nupercainal, generic) number equals 40-60
    • Moderately prolonged duration-- as long as 30 minutes following succinylcholine (Anectine)
  • Dibucaine (Nupercainal, generic) analysis only measures enzyme capability for succinylcholine (Anectine) hydrolysis--
    • reduced active enzyme {due to affects the liver disease [reduced synthesis] or enzyme inhibition due to anticholinesterases} will affect succinylcholine (Anectine) duration, but not be detected by dibucaine (Nupercainal, generic) analysis

Miller, R.D., Skeletal Muscle Relaxants, in Basic and Clinical Pharmacology, (Katzung, B. G., ed) Appleton-Lange, 1998, pp 434-449. Stoelting, R.K., "Neuromuscular-Blocking Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, pp 182-219 White, P. F. "Anesthesia Drug Manual", W.B. Saunders Company, 1996.​

 

[BLADEMDA]

Return of neuromuscular function after neostigmine is the sum of spontaneous recovery from the relaxant and its acceleration by the reversal drug (14). Spontaneous recovery is a function of a decrease in the concentration of relaxant at the neuromuscular junction. The in vitro recovery (and onset) from NMB induced by iontophoretic administration is related to the potency of the NMB drug and is likely the consequence of the rate of removal of drug from the receptor by processes such as "buffered diffusion." Consequently, the poorly potent rocuronium has a more rapid onset and recovery than do other nondepolarizing relaxants (15). In clinical practice, a decrease in receptor concentration may also be affected by the rate of peripheral distribution (rapacuronium) [x](16), organ disposition (rocuronium, atracurium), decomposition (atracurium, cisatracurium), and metabolism (mivacurium). Pharmacokinetically, after the administration of single boluses of most nondepolarizing relaxants, distribution is more important than metabolism or excretion in determining the rate of recovery, except when the latter form a major route of elimination (mivacurium, atracurium, and cisatracurium). Hence, NMB drugs with similar terminal half-lives (e.g., pancuronium and vecuronium) may have different rates of spontaneous recovery because recovery takes place during the distribution phase for vecuronium and during the elimination phase for pancuronium (17). Administration of the anticholinesterase neostigmine increases the junctional concentration of acetylcholine, the drug unbound to the receptor may increase and diffuse from the junction. The rate of restoration of neuromuscular function after neostigmine administration is affected by the level of block at the time of reversal (18–21), choice and dose of relaxant and reversal drugs (22), and drug interactions [inhaled anesthetics (23), and anticonvulsants].