Do we need narcotics in anesthesia?

[sevoflurane]

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Kinda tangential but anybody using methadone out there? Had a few who used it in residency and I liked what it got you- nice smooth profile, some NMDA antagonism, and long duration. None of my current shops have it IV unfortunately. Would be nice for big cases- back whacks, etc.

Yes. HB. Good stuff for the spine cases.

 

[deleted9493]

I like methadone for big spine cases, if the surgeon isn't willing to drop an epidural catheter. Epidural catheters in those patients are hard to beat. Many with 0/10 pain when the rate is titrated to effect. As far as methadone goes, I'll give .25mg/kg on arrival to the room and re-dose after 4hrs (as opposed to running an infusion), if we're going to be on the table intubated for another hour or more. It's easy to titrate just before or after extubation because of its quick onset. The downside being that you're stuck with the side effects longer than you are with shorter duration opioids, adding further caution to its titration. http://onlinelibrary.wiley.com/doi/10.1111/pan.12021/abstract

I have used low dose dexmedetomidine infusions (.2 mcg/kg/h, using actual weight) on morbidly obese patients having laparoscopic bypass surgeries or hernia repairs. Half a MAC of desflurane. That's about all I have to give for the case and they seem to do well for the first 4-6hrs. I'd be comfortable using that technique with TAP blocks for an open hernia.

Thanks for the tips on esmolol and magnesium!

 

[deleted162650]

So I'm pretty intrigued w/ esmolol as an adjunct, but my question is:

Is there something special about esmolol, or does the same apply to any B-blocker? Would some labetalol or metoprolol have the same effect?

 

[Noyac]

So I'm pretty intrigued w/ esmolol as an adjunct, but my question is:

Is there something special about esmolol, or does the same apply to any B-blocker? Would some labetalol or metoprolol have the same effect?

That is the question. I have been using more and more metoprolol over the past few years partly for this reason so I believe that it may be a universal. But I have no "real" proof.

 

[Noyac]

A couple studies if interested:
http://scholar.google.com/scholar?q...a=X&ei=x2dYU-mrFtW0yASrqoLAAQ&ved=0CCgQgQMwAA

Possible mechanism: Inhibitory G protein-coupled receptor agonists act on post-synaptic inhibition via G protein-coupled potassium channels or via the pre-synaptic inhibition of neurotransmitter release through the regulation of voltage-gated Ca2+ channels; such a pathway underlies the antinociceptive effect of clonidine

The case for metoprolol and labetalol:
β-blockers, which decrease hepatic opioid metabolism and lengthen the analgesic effect, are limited only to those metabolized by the liver. For example, propranolol decreases its own metabolism and that of certain other drugs by eliciting a reduction in hepatic blood flow. This could affect the metabolism of drugs with a large hepatic extraction ratio, such as fentanyl, and it would seem likely that propranolol use would result in prolonging the analgesic effect of fentanyl and also elicit a reduction in postoperative opioid consumption

 

[rsgillmd]

There has to be a secondary mechanism. Esmolol is metabolized by RBC esterases, not liver. I always thought it was due to dampening the sympathetic system which can be in overload in pain (similar to what you are describing for clondine).

A couple studies if interested:
http://scholar.google.com/scholar?q=esmolol postoperative pain&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ei=x2dYU-mrFtW0yASrqoLAAQ&ved=0CCgQgQMwAA

Possible mechanism: Inhibitory G protein-coupled receptor agonists act on post-synaptic inhibition via G protein-coupled potassium channels or via the pre-synaptic inhibition of neurotransmitter release through the regulation of voltage-gated Ca2+ channels; such a pathway underlies the antinociceptive effect of clonidine

The case for metoprolol and labetalol:
β-blockers, which decrease hepatic opioid metabolism and lengthen the analgesic effect, are limited only to those metabolized by the liver. For example, propranolol decreases its own metabolism and that of certain other drugs by eliciting a reduction in hepatic blood flow. This could affect the metabolism of drugs with a large hepatic extraction ratio, such as fentanyl, and it would seem likely that propranolol use would result in prolonging the analgesic effect of fentanyl and also elicit a reduction in postoperative opioid consumption

 

[BuzzPhreed]

There has to be a secondary mechanism. Esmolol is metabolized by RBC esterases, not liver. I always thought it was due to dampening the sympathetic system which can be in overload in pain (similar to what you are describing for clondine).

I mentioned this earlier in this thread. There has been work done with propanolol. This study was just completed: http://clinicaltrials.gov/show/NCT01094574

 

[rsgillmd]

Must have missed it. Post-call this morning. Thanks for the link.

 

[Noyac]

There has to be a secondary mechanism. Esmolol is metabolized by RBC esterases, not liver. I always thought it was due to dampening the sympathetic system which can be in overload in pain (similar to what you are describing for clondine).

Yes, esmolol is metabolized differently and it's contribution to pain control may be explained by my "possible mechanism" quote above.

 

[soorg]

When using methadone for spine cases, are you supplementing it with any additional opioids? Are you good enough (for four hours) with just the methadone?

 

[kazuma]

Thanks for the tips, I've been trying the magnesium as an adjuvant over the past week. My limited anecdotal experience with it has been promising as it seems to help decrease opioid requirements. I've been using it with one or more adjuvants including decadron, ketamine, toradol, and IV acetaminophen. It seems like I've been using much less narcotic, usually just 50-150 MCG of fentanyl (sometimes none) for most cases. I've been reading about magnesium and some studies have suggested that in combination, magnesium and ketamine have a synergistic effect on MDMA antagonism. While the analgesic properties of magnesium are controversial, there seems to be evidence to suggest that a 50mg/kg magnesium bolus can lead to less post-op pain and reduced opioid consumption.

One of the most interesting cases was a ~60F 5-level thoracic spine fusion. I used remi @ 0.3 mcg/kg/min, 100mg lido, and 40mg propofol for induction (2mg versed in pre-op). Maintenance was ketamine @ 0.4-0.6mg/kg/hr until the hardware was placed, and a propofol/remi titrated TIVA throughout the case. I gave 3 grams magnesium, 10mg decadron, and acetaminophen IV @15mg/kg after induction. I only used 50mcg of fentanyl 20-30 minutes before arrival in PACU. Super smooth wakeup/extubation within a couple minutes of turning supine. Checked up 30 minutes later in PACU and she was still comfortable and hadn't received any other opioids. My attending even commended me and made a big deal about how smooth the anesthetic was in front of the OR staff and neurosurgeons. Most of the evidence suggest virtually no unwanted side effects of magnesium (50mg/kg bolus) and possibly some significant benefits.

Here's meta-analysis from Anesthesiology last year that supports the use of magnesium as a pain adjuvant:

Anesthesiology:
July 2013 - Volume 119 - Issue 1 - p 178–190
doi: 10.1097/ALN.0b013e318297630d
Pain Medicine
Perioperative Systemic Magnesium to Minimize Postoperative Pain: A Meta-analysis of Randomized Controlled Trials