MgSO4 as analgesia?

[McPoyle]

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After reading some recent posts on here I decided to explore using magnesium as an adjunct for analgesia. I was on call last night and had exlap for SBO. I did some brief research during the case and found various regimens people tried and for ease I went with the single bolus of 50mg/kg. My staff (I'm a CA3) were a little nervous as this ended up being 4g based on estimated weight of 80kg. Ended up getting 50mcg of fentanyl at induction, 100mcg around incision and 0.5mg dilaudid on emergence as well as 15mg ketorolac (had been giving 30 but another recent thread made me re-evaluate). Seemed decently comfy in pacu (though crazy from the get go) and did not require narcs until she got her PCA from surgery.

So, my question is:
For those ho use magnesium regularly or have good experience with it, what regimen are you using? Are there populations where you do not see a benefit (one metanalysis suggested GI surgery showed no benefit)?

Thanks in advance, and thanks for proving a valuable resource!


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[Hoya11]

After reading some recent posts on here I decided to explore using magnesium as an adjunct for analgesia. I was on call last night and had exlap for SBO. I did some brief research during the case and found various regimens people tried and for ease I went with the single bolus of 50mg/kg. My staff (I'm a CA3) were a little nervous as this ended up being 4g based on estimated weight of 80kg. Ended up getting 50mcg of fentanyl at induction, 100mcg around incision and 0.5mg dilaudid on emergence as well as 15mg ketorolac (had been giving 30 but another recent thread made me re-evaluate). Seemed decently comfy in pacu (though crazy from the get go) and did not require narcs until she got her PCA from surgery.

So, my question is:
For those ho use magnesium regularly or have good experience with it, what regimen are you using? Are there populations where you do not see a benefit (one metanalysis suggested GI surgery showed no benefit)?

Thanks in advance, and thanks for proving a valuable resource!


Sent from my iPad using SDN mobile

In those with an active pulse, Mg showed no benefit for pain..

Seriously though, for acute pain I think mag has absolutely no role, for chronic pain it only has a role of making money for the pain doctor while a crazy "CRPS" patient gets an infusion 3x per week in your ASC. Mag is old, dirty, ineffective. Literature that says it works should open your eyes to how easy it is to formulate a positive study for analgesica. Take a look at the patients response to it, see it you think it helps their pain. It may just obtund them at best

 

[Aether2000]

There are some good controlled studies showing post op pain improved by intraoperative IV administration of magnesium:
https://www.ncbi.nlm.nih.gov/pubmed/27648185
https://www.ncbi.nlm.nih.gov/pubmed/27687417
When added to bupivicaine in a 3 in 1 block: https://www.ncbi.nlm.nih.gov/pubmed/27512165
Intraop bolus followed by IV infusion postop: https://www.ncbi.nlm.nih.gov/pubmed/27435514
IM in paraspinous muscles with back surgery: https://www.ncbi.nlm.nih.gov/pubmed/27022607
It does not work in sickle cell or visceral pain....

 

[Planktonmd]

Magnesium is an excellent sedative and muscle relaxant and these 2 things will improve the quality of your anesthetic.
Magnesium also antagonizes NMDA receptors so this might help in analgesia and decreasing opiate consumption.
Is it a better analgesic than other adjuncts like NSAIDS, Acetaminophen, Gabapentin, Ketamine...? Probably not!

 

[Noyac]

I obviously like to use Mg as I have stated here on many occasions. Just don't expect miracles from it.
My approach is 2gm intraop over 10-30 min.
Then if the pt needs more pain control in PACU which is admittedly rare I will give another 2gm over the same 10-30 min.
It is used to augment your other forms of pain control.

 

[sevoflurane]

Yes Mag works for analgesia. I will 2nd Noy's assertion of Mags ability to augment other analgesics.

 

[Noyac]

Yes Mag works for analgesia. I will 2nd Noy's assertion of Mags ability to augment other analgesics.

Finally, some support on this site. 😉

 

[deleted162650]

Since we last talked about Mg for analgesia I've experimented with it in a couple of cases - both chronic pain patients. I've done it both intra-op and as a PACU "rescue" administered as above. From my extensive experience I'd have to agree that it does work, and I'll continue to use it as an adjunct in the opioid tolerant chronic painers that need a little NMDA action (in addition to low dose ketamine).

 

[pgg]

I am also a fan of Mg++ as an adjunct.

 

[dhb]

In those with an active pulse, Mg showed no benefit for pain..

Seriously though, for acute pain I think mag has absolutely no role, for chronic pain it only has a role of making money for the pain doctor while a crazy "CRPS" patient gets an infusion 3x per week in your ASC. Mag is old, dirty, ineffective. Literature that says it works should open your eyes to how easy it is to formulate a positive study for analgesica. Take a look at the patients response to it, see it you think it helps their pain. It may just obtund them at best

 

[McPoyle]

Magnesium is an excellent sedative and muscle relaxant and these 2 things will improve the quality of your anesthetic.
Magnesium also antagonizes NMDA receptors so this might help in analgesia and decreasing opiate consumption.
Is it a better analgesic than other adjuncts like NSAIDS, Acetaminophen, Gabapentin, Ketamine...? Probably not!

And this was my goal, as an adjunct to reduce the narcotic demand in conjunction with other things.

It sounds like the prevailing regimen is 2g intraoperatively around here, is there anything y'all do in regards to timing of the dose?


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[Hoya11]

I have no shame about going on the record and stating that I dislike Mg++, Lido infusions, Ketamine infusions.. I think they all do nothing (or next to nothing) for the patient and make your anesthetic more cumbersome. Maybe ketamine makes you run a little less propofol but who cares? I still have to set up the ketamine and expose the patient to a strange experience potentially. I think they are theoretical analgesics more than actual ones. I think precedex and Nitrous (my NMDA of choice) are much better adjuvants than all of the above. Like any study trying to objectify the subjectivity of pain, take them with a grain of salt. If you clinically think that patients are doing better on these medications, vs nitrous and precedex, from what you are seeing with your own eyes, then all I can say is agree to disagree.

 

[BLADEMDA]

I have no shame about going on the record and stating that I dislike Mg++, Lido infusions, Ketamine infusions.. I think they all do nothing (or next to nothing) for the patient and make your anesthetic more cumbersome. Maybe ketamine makes you run a little less propofol but who cares? I still have to set up the ketamine and expose the patient to a strange experience potentially. I think they are theoretical analgesics more than actual ones. I think precedex and Nitrous (my NMDA of choice) are much better adjuvants than all of the above. Like any study trying to objectify the subjectivity of pain, take them with a grain of salt. If you clinically think that patients are doing better on these medications, vs nitrous and precedex, from what you are seeing with your own eyes, then all I can say is agree to disagree.

I use ketamine all the time. But, my KISS technique is a small bolus upfront (that's it) or I'll add it to the propofol infusion syringe for big neuro case which utilizes neuromonitoring.

 

[Noyac]

I have no shame about going on the record and stating that I dislike Mg++, Lido infusions, Ketamine infusions.. I think they all do nothing (or next to nothing) for the patient and make your anesthetic more cumbersome. Maybe ketamine makes you run a little less propofol but who cares? I still have to set up the ketamine and expose the patient to a strange experience potentially. I think they are theoretical analgesics more than actual ones. I think precedex and Nitrous (my NMDA of choice) are much better adjuvants than all of the above. Like any study trying to objectify the subjectivity of pain, take them with a grain of salt. If you clinically think that patients are doing better on these medications, vs nitrous and precedex, from what you are seeing with your own eyes, then all I can say is agree to disagree.

Well like I said a few weeks ago. I had ketamine not long ago and it is a different feeling. I know this because I've had many surgeries and I received ketamine twice. It isn't something you forget but it isn't anything bad either. It's just different. I even doubt the average pt would even know there was a difference. Maybe my high school and college days prepared me for this. IDK.
But this last surgery should have been at least somewhat painful. It wasn't. It was nearly painless. It was a THA, anterior approach. It was impressively painless. The ACL was way worse. Infinitely worse.
Was it the ketamine, I have no idea. I am known for not feeling pain much so that helps. And it takes a lot of painful events to be given this distinction.
To be clear, I believe nearly all physicians are extremely tolerant of pain. They understand it well so they are a poor indicator of adjuvant therapy.

 

[dhb]

I have no shame about going on the record and stating that I dislike Mg++, Lido infusions, Ketamine infusions..

Ok i don't do infusion either. I always mix sufenta with ketamine to 4mcg/10mg per ml.
I reserve magnesium for pacu rescue.
I'm sure that you've had the patient that complains of pain in the pacu despite an adequate analgesia regimen. If you give that patient 2 or 3g of mag, i've seen that 100% of the time you get a decrease in pain level to a point where you can discharge them from pacu.
So try it next time and become a believer.

 

[Noyac]

One of the best articles I've read in a while regarding pain and our approach to it:

http://www.medscape.com/viewarticle/869056_2


Transmission (Synaptic Transfer of Generated Electrical Activities From One Neuron to Another From Periphery to Higher Centers Through Spinal Tracts)
Neurotransmitters of the majority of interneurons are gama-aminobutyric acid (GABA) and glycine both of which are inhibitory in action. The main excitatory amino acid is alpha amino-3-hydroxy-5-methyl-4-isozole propionic acid (AMPA/kinate receptor) located at the post-synaptic to primary afferent fibers. It is important to note that N-methyl-D-aspartate (NMDA) receptors are postsynaptic to interneurons and the AMPA/kinate and substance-P must be activated prior to NMDA receptor activation.[11,15] The first event at a molecular level in the dorsal horn is release of excitatory amino acids like glutamate and aspartate from primary afferent fiber nerve endings (Figure 2). They bind to AMP/kinate receptors leading to the opening of ion channels and depolarization of second order neurons. These voltage sensitive events remove a magnesium plug responsible for keeping NMDA receptors in an inactive state. Glycine binding also takes place to finally activate NMDA receptors.

(Enlarge Image)
Figure 2.



Role of N-methyl-D-aspartate (NMDA) receptor in hyperalgesia, central sensitization and opiate tolerance.



Now a complex cascade of events occurs, which includes marked release of intracellular calcium, which then activates phospholipase-A2, enhances PG production and increases production of substance-P. NMDA activation also causes release of nitric oxide (NO). Both PG and NO diffuse extracellularly to induce primary afferent neurons and release excitatory neurotransmitters. It is believed that once the cascade of events is initiated, the blockade of peripheral nociceptor input fails to completely stop dorsal horn neurons from firing. This wind-up phenomenon leads to clinical sequelae of hyperalgesia, muscle spasm, allodynia, increased sympathetic tone, and subsequent decrease in blood flow.[16–18] Higher doses of analgesics such as opiates are required to suppress the pain, and hence NMDA receptors are implicated in the development of opiate tolerance. This also explains why long standing pain syndrome fails to improve even after surgical intervention and correction of primary anatomic abnormality. This is responsible for chronic pain and pain syndrome even after successful TKR in some patients who have had severe long-term osteoarthritis pain. NMDA receptors also are held responsible for the complex phenomenon of central sensitization (ability of benign and low-threshold stimuli to activate second order neurons) if afferent nerve stimulation is intense and of sufficient duration.[4,11–13,15]

 

[DrN2O]

I have no shame about going on the record and stating that I dislike Mg++, Lido infusions, Ketamine infusions.. I think they all do nothing (or next to nothing) for the patient and make your anesthetic more cumbersome.

What do you do for complex spines with neuromonitoring? I like the KISS approach, but there's no way to get around these cases. I guess that's why I have residents and CRNAs.

 

[GasOrBust]

I recently did an opioid-free anesthetic on a young adult spine case. She had allergies to multiple opioids and a history of PONV, but mainly I was just curious to give it a shot and see how it worked. Infusions of lidocaine, ketamine, precedex plus acetaminophen and toradol. Bolused ketamine with intubation and incision. Woke up beautifully. Checked on her in PACU later and still hadn't asked for any pain meds.

I'm a big fan of ketamine and frequently give some along with a little long-acting opioid several minutes before incision. I usually see no change in vitals signs when they cut.

 

[Hoya11]

What do you do for complex spines with neuromonitoring? I like the KISS approach, but there's no way to get around these cases. I guess that's why I have residents and CRNAs.

1/2 Mac Volatile, 1/2 Mac Propofol, Dilaudid boluses, fentanyl boluses. Precedex if huge narcotic tolerance. ETCO2 30. KISS

 

[BLADEMDA]

What do you do for complex spines with neuromonitoring? I like the KISS approach, but there's no way to get around these cases. I guess that's why I have residents and CRNAs.

I use 1/2 MAC volatile agent and propofol mixed with ketamine. Narcotics are reduced with the addition of the ketamine in the propofol.

For those patients taking huge amounts of narcotics prior to surgery I suggest methadone as part of the anesthetic plan:

https://www.ncbi.nlm.nih.gov/pubmed/20418538

http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2210048

 

[Noyac]

ETCO2 30. KISS

Why ETCO2 @ 30?

 

[Hoya11]

Why ETCO2 @ 30?

so they dont try to come back breathing


NMDA receptor antagonists are interesting. The physiology and pathways are relatively new and interesting. Seeing and treating patients with "wind up" or CRPS is interesting. It all makes you think. But the reality is, most patient diagnosed with CRPS/wind up are inappropriately diagnosed. And true CRPS/wind up is VERY rare.

Also, its not as simple as just the NMDA receptor involved. Current research shows there are other receptors (some andrenergic some other strange types) involved in CRPS maybe to more of a degree than NMDA. The wind up pathway is still being figured out.

So to sum up, I think the return on investment of bombing the general population with NMDA receptor anatagonist drugs is very low. Due to the incidence of CRPS being so rare and due to unclear role of each drug in that overall disease. At some point there is more of a risk of side effects than potential benefit.

Whos to say waking up on nitrous is less beneficial than that ketamine in the propofol? We really dont know. Its trendy right now to choose these drugs (ie methadone instead of oxycontin/ms contin) But IMO its a lot of talk/hub ub for a very rare and poorly understood problem

 

[Noyac]

so they dont try to come back breathing

I thought so. Isn't that what the dilaudid is for?

 

[Aether2000]

The idea of multimodal analgesia was pushed hard at the PGA this year. There is mounting evidence that several intraoperative measures (including intraop magnesium) can reduce post op opioid consumption significantly during the first 1-2 days. For those of us that have practiced pain management for several years, it has become obvious that the reduction or elimination of opioids for acute pain eliminates the chemical dependency that occurs in chronic pain. Therefore any measures that can be taken (including bolus intraoperative ketamine, intraop IV NSAIDS, regional blocks, regional catheters, IV magnesium, intraoperative clonidine, early application of ice, preop discussion of expected pain and the measures that will be used to mollify the anxiety and ameliorate the pain, etc) may have long term benefits through early reduction of high dose opioids that are often applied in the PACU and after discharge. The avoidance of these high dose opioids early on may reduce the creation of chemical dependency/addiction later on. We can make a difference- provided the surgeons can curtail their lust for overprescribing of opioids after surgery.

 

[CopaceticOne]

Random question: Do any of you know what a patient's serum Mg level is prior to giving it? I'm asking because my experience thus far is there a a fairly sizable number of patients with some level of Mg deficiency. I'm wondering if the 2gm of Mg isn't making some difference because of basic repletion effects vs the MG itself.

 

[BLADEMDA]

Magnesium is the fourth most abundant mineral in your body, yet an estimated 80 percent of Americans are deficient in it. Without sufficient amounts of magnesium your body simply cannot function at its best. Insufficient cellular magnesium levels set the stage for deterioration of proper metabolic function that typically snowballs into more significant health problems. Researchers have detected more than 3,750 magnesium-binding sites on human proteins,6 reflecting how important this mineral is to a great many biological processes.


Proton pump inhibitors
Prescription proton pump inhibitor (PPI) drugs, such as esomeprazole magnesium (Nexium®) and lansoprazole (Prevacid®), when taken for prolonged periods (typically more than a year) can cause hypomagnesemia [62]. In cases that FDA reviewed, magnesium supplements often raised the low serum magnesium levels caused by PPIs. However, in 25% of the cases, supplements did not raise magnesium levels and the patients had to discontinue the PPI. FDA advises healthcare professionals to consider measuring patients' serum magnesium levels prior to initiating long-term PPI treatment and to check magnesium levels in these patients periodically [62].