Physostigmine + Neostigmine

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During my pediatric rotation I worked with a CRNA that routinely uses a combination of neostigmine and physostigmine for older children & adolescents. She calculates her normal neostigmine reversal dose but only gives 2/3 of it and the other 1/3 as physostigmine. For example, a 40kg pt may require 2.4mg of neostigmine but she only gives 1.6mg while giving the other 0.8mg as physostigmine. She states that these patients wake up "smoother" than those receiving just neostigmine but has no solid reasoning for doing so. Apparently she learned this from her preceptor many years ago. I understand that physostigmine has a tertiary amino group that passes the blood brain barrier but this patient population doesn't necessarily receive any anticholinergic that passes the barrier (e.g. Atropine).

Does anybody have any insight on this?

Thanks.

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doesn't make any sense...another example of voodoo anesthesia. sad.

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If it's comfortable for the patient, does it have to be sad?

just playing devil's advocate. I realize it's not evidence based medicine.

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Bogus all around. Physostigmine is not indicated for reversal of NMB. Any chance you're thinking of pyridostigmine, which is a pretty old drug we used to use eons ago?

And if you have "no solid reasoning for doing so", why the hell would you give it, or anything else for that matter? It has nothing to do with being "comfortable for the patient" (where did that come from?)

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Hate to disagree with you, jwk, but physostigmine is, of course, a cholinesterase inhibitor, and has LONG been used as a reversal agent - don't know where you came up with idea that it has no indications as one. That being said....I certainly don't see it being used much these days at all, and have not seen any combinations as described above. Devine....sounds like an interesting mini-research project......My guess is that you will find most clinicians don't use it at all anymore. Good luck!

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Hate to disagree with you, jwk, but physostigmine is, of course, a cholinesterase inhibitor, and has LONG been used as a reversal agent - don't know where you came up with idea that it has no indications as one. That being said....I certainly don't see it being used much these days at all, and have not seen any combinations as described above. Devine....sounds like an interesting mini-research project......My guess is that you will find most clinicians don't use it at all anymore. Good luck!

OK, an ACH inhibitor it is, but in 25 years, I've never seen it used for reversing NMB's. I've got a few old-fashioned tricks up my sleeve as well, but this isn't one of them.

However, I'll stand by my statement that if you have "no solid reasoning for doing so" then you shouldn't be giving any drug or treatment. If you don't have a reason for, or understand why you're doing what you're doing, then don't do it. And just doing it because someone else told you it was neat to do years ago? Not a good reason either.

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OK, an ACH inhibitor it is, but in 25 years, I've never seen it used for reversing NMB's. I've got a few old-fashioned tricks up my sleeve as well, but this isn't one of them.

However, I'll stand by my statement that if you have "no solid reasoning for doing so" then you shouldn't be giving any drug or treatment. If you don't have a reason for, or understand why you're doing what you're doing, then don't do it. And just doing it because someone else told you it was neat to do years ago? Not a good reason either.

Well, jwk...jes take a peek at any good anesthesia reference, and there you will find it. Funny what a good read will do.

Could be me, but you sound a little defensive. I think anybody would agree that good practice should have solid reasoning behind it. Devine was just asking a question....and that is exactly what students should be doing, and encouraged to do. Keep asking, Devine!

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Thanks for the replies! The use of physostigmine isn't my choice of routine neuromuscular blockade reversal and I've never chosen to give it over others.

The CRNA that shared this technique with me certainly has her reasoning for using it, but it is my intention to find out why it may or may not work. Obviously I don't just reach in the drug tray and give drugs without knowing all appropriate indications; but, if there are "tricks" that people have passed down over the years, I don't mind investigating one's reasoning before accepting it.

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Thanks for the replies! The use of physostigmine isn't my choice of routine neuromuscular blockade reversal and I've never chosen to give it over others.

The CRNA that shared this technique with me certainly has her reasoning for using it, but it is my intention to find out why it may or may not work. Obviously I don't just reach in the drug tray and give drugs without knowing all appropriate indications; but, if there are "tricks" that people have passed down over the years, I don't mind investigating one's reasoning before accepting it.

Is the practioner using atropine or robinul in the mix? That might explain the physostigmine.

Mike

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this patient population doesn't necessarily receive any anticholinergic that passes the barrier (e.g. Atropine).

Does anybody have any insight on this?

Thanks.

What is the dose of atropine?

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during my pediatric rotation i worked with a crna that routinely uses a combination of neostigmine and physostigmine for older children & adolescents. she calculates her normal neostigmine reversal dose but only gives 2/3 of it and the other 1/3 as physostigmine. for example, a 40kg pt may require 2.4mg of neostigmine but she only gives 1.6mg while giving the other 0.8mg as physostigmine. she states that these patients wake up "smoother" than those receiving just neostigmine but has no solid reasoning for doing so. apparently she learned this from her preceptor many years ago. i understand that physostigmine has a tertiary amino group that passes the blood brain barrier but this patient population doesn't necessarily receive any anticholinergic that passes the barrier (e.g. atropine).

does anybody have any insight on this?

thanks.

you might want to grab this article from your library (pubmed will answer many of your questions)

acta anaesthesiol scand. 1981 oct;25(5):387-90.[color=#336699]related articles, [color=#336699]links

comparison of physostigmine and neostigmine for antagonism of neuromuscular block.

salmenpera m, nilsson e.

the ability of physostigmine alone and in combination with neostigmine to reverse d-tubocurarine-induced neuromuscular block was evaluated in surgical patients. the relaxation was maintained at a level of 90% twitch suppression during balanced anesthesia, and antagonism was attempted with physostigmine 1.5 mg x 3; neostigmine 0.5 mg x 3; neostigmine 1.0 mg x 3; or with a combination of physostigmine 0.75 mg and neostigmine 0.5 mg x 3. the measured parameters included the twitch force or emg amplitude of the adductor pollicis brevis muscle after supramaximal 0.1 hz stimulation and fading of these responses after repetitive 2 and 50 hz stimuli. although the restitution rate of twitch height and emg amplitude were essentially the same with both antagonists, there was a considerable time-lag in regeneration of the fades after repetitive stimuli with physostigmine as compared with the neostigmine group. the addition of physostigmine to a subeffective dose of neostigmine resulted in antagonism comparable to that seen in other groups. the clinical antagonism was satisfactory in all patients receiving physostigmine. the divergence of relaxation-indicating parameters (twitch responses and fades) after physostigmine suggests dissimilar modes of action of two antagonists at the neuromuscular junction

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you may also want to review this article, it states a couple of reasons why physotigmine might be useful.

anaesthesiol reanim. 1989;14(4):235-41.[color=#336699]related articles, [color=#336699]links

[physostigmine--recent pharmacologic data and their significance for practical use]

[article in german]

rupreht j, schneck hj, dworacek b.

physostigmine is widely used for treatment of the central anticholinergic syndrome during recovery from anaesthesia. the drug is also very useful in treatment of intoxicated patients, in differential-diagnostic procedures of coma of unknown origin, and in restoration of vigilance after prolonged sedation for mechanical ventilation. besides the specific central cholinergic action of physostigmine, several new pharmacological actions have now been established. analgesic action is dependent on the interaction with the 5-ht (serotoninergic) system and is independent of narcotic or cholinergic agonists. the antianalgetic stress hormone, acth, also does not interfere with this action. physostigmine does not interfere with the anaesthetic state when given during general anaesthesia. it attenuates several withdrawal states, especially alcohol delirium, opiate and nitrous oxide withdrawal syndromes. the drug may offer a protective mechanism against hypoxic damage of the brain and may also be beneficial in amnestic syndromes and sleep disorders. physostigmine produces central and peripheral cardiovascular stimulation. it has been shown that physostigmine can be useful in prevention and treatment of postanaesthetic behavioural disturbances following anaesthesia with propofol. number of indications for use of physostigmine has increased considerably

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