dexmedetomidine & MEPs

[turnupthevapor]

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Our monitoring dude was giving us a hard time about using preceded for MEP cases the other day....claimed it gives false positives

any feedback??



Paediatr Anaesth. 2008 Nov;18(11):1082-8. doi: 10.1111/j.1460-9592.2008.02733.x.
Effects of dexmedetomidine on intraoperative motor and somatosensory evoked potential monitoring during spinal surgery in adolescents.
Tobias JD1, Goble TJ, Bates G, Anderson JT, Hoernschemeyer DG.
Author information:
1Department of Anesthesiology, University of Missouri, Columbia, MO 65212, USA. [email protected]

Abstract
BACKGROUND:
Dexmedetomidine may be a useful agent as an adjunct to an opioid-propofol total intravenous anesthesia (TIVA) technique during posterior spinal fusion (PSF) surgery. There are limited data regarding its effects on somatosensory (SSEPs) and motor evoked potentials (MEPs).

METHODS:
The data presented represent a retrospective review of prospectively collected quality assurance data. When the decision was made to incorporate dexmedetomidine into the anesthetic regimen for intraoperative care of patients undergoing PSF, a prospective evaluation of its effects on SSEPs and MEPs was undertaken. SSEPs and MEPs were measured before and after the administration of dexmedetomidine in a cohort of pediatric patients undergoing PSF. Dexmedetomidine (1 microg x kg(-1) over 20 min followed by an infusion of 0.5 microg x kg(-1) x h(-1)) was administered at the completion of the surgical procedure, but prior to wound closure as an adjunct to TIVA which included propofol and remifentanil, adjusted to maintain a constant depth of anesthesia as measured by a BIS of 45-60.

RESULTS:
The cohort for the study included nine patients, ranging in age from 12 to 17 years, anesthetized with remifentanil and propofol. In the first patient, dexmedetomidine was administered in conjunction with propofol at 110 microg x kg(-1) x min(-1) which resulted in a decrease in the bispectral index from 58 to 31. Although no significant effect was noted on the SSEPs (amplitude or latency) or the MEP duration, there was a decrease in the MEP amplitude. The protocol was modified so that the propofol infusion was incrementally decreased during the dexmedetomidine infusion to achieve the same depth of anesthesia. In the remaining eight patients, the bispectral index was 52 +/- 6 at the start of the dexmedetomidine loading dose and 49 +/- 4 at its completion (P = NS). There was no statistically significant difference in the MEPs and SSEPs obtained before and at completion of the dexmedetomidine loading dose.

CONCLUSION:
Using the above-mentioned protocol, dexmedetomidine can be used as a component of TIVA during PSF without affecting neurophysiological monitoring.

PMID: 18717802 [PubMed - indexed for MEDLINE]

 

[somedumbDO]

I used it a lot in pedi spines never had an issue. Tell the nerve monitoring tech to mind his own business. I had one in training that said des effected ssep. Her experience was n=1 with a resident running 1.5 Mac of gas. I just turned the monitor away so she cudnt see it, and asked if baselines were good. Remember these are techs u r a doc.

 

[nap$ter]

your tech is right - you should not use dexmed in cases with neuromonitoring.

initial data made it look ok, but multiple subsequent studies have demonstrated markedly reduced signals with dexmed. i think most of the papers were in Anesthesiology.

 

[somedumbDO]

your tech is right - you should not use dexmed in cases with neuromonitoring.

This study initial data made it look ok, but multiple subsequent studies have demonstrated markedly reduced signals with dexmed. i think most of the papers were in Anesthesiology.

Yeah I read the article but this study had some huge weak points as discussed by an editorial below. My n=100 ish w pedi spines says its ok w meps and definitely ok w sseps. The literature is pretty clear as to no issues w sseps. They are finishing a large study next month with regards to meps and precedex and this should give some better info.

For your reading pleasure the editorial.

Some caveats should be considered. First, the study had planned to recruit 72 patients, but only 40 patients completed the study. The study actually had to be terminated early because a change occurred of surgical technique during the study period. The group utilized a pharmacokinetic model from Petroz et al. [1] to estimate target based plasma dexmedetomidine levels. The study the authors based their infusion rates on by Petroz et al. was created in pediatric patients aged 2 yr to 12 yr. The age group in the present study ranged from 10 yr to 25 yr. As pharmacokinetics may differ in a two year old from that of a 25 year old, the question arises as to how reliable the target plasma levels of dexmedetomidine were in the present study. Furthermore, the Petroz study only had 36 patients, far from a robust study to given reliable plasma drugs levels based on a predetermine infusion rate. The plasma levels chosen were 0.4 ng/ml and 0.8 ng/ml for the low and high dex groups respectively. They did the same for propofol. They do not provide us good insight as to what infusion rates were utilized to acheive the target plasma levels cited in the study (i.e. 0.4 ng/ml and 0.8 ng/ml). Although the authors did randomly take plasma samples to verify that the pharmacokinetic model they were using was accurate, there is a small chance that some patients deviated from the target plasma drug level of dex. The small number of patients creates further risk of varying plasma levels disrupting an statistical analysis.
Their study did seem to match the results of two previous studies looking on the effect of dexmedetomidine in neuromonitoring in that SSEPs were not affected at all even at higher dexmedetomidine dosages.[2,3] The previous studies, however, concluded that dexmedetomidine did not effect MEPs in a clinically relevant matter. One of the studies (Bala et al.) utilized two target plasma levels for dex (0.3 ng/ml and 0.6 ng/ml). Once again, one can only wonder if the actual plasma levels of dex in the present study were as claimed. The authors of the current study claim to confirm the results of the other study listed [3], but then state, "...Whereas the other eight patients do not fit into any of our experimental groups as the computed propofol effect site concentration is less than that targeted in our group 2." Tobias looked at 9 patients who received a propofol infusion w/ BIS monitoring. Dexmedetomidine was loaded with a dosage of 1 mcg/kg over 20 minutes. This would provide a plasma concentration per the authors of the present study of 0.84 ng/ml (the same as their high dex group). The first patient in the protocol had a BIS decrement from 58 to 31 indicating overdosage of anesthesia. The protocol in Tobias et al. was then modified to decrease the propofol infusion to maintain a stable BIS as dexmedetomidine was added. Although the MEPs did decrease in the first patient, it was likely a result of very deep anesthesia, and the next eight patients in the Tobias study did not experience a significant decrement in MEPs with dexmedetomidine. The other patients had their BIS maintained at about 50.

 

[nap$ter]

Yeah I read the article but this study had some huge weak points as discussed by an editorial below. My n=100 ish w pedi spines says its ok w meps and definitely ok w sseps. The literature is pretty clear as to no issues w sseps. They are finishing a large study next month with regards to meps and precedex and this should give some better info.

For your reading pleasure the editorial.

Some caveats should be considered. First, the study had planned to recruit 72 patients, but only 40 patients completed the study. The study actually had to be terminated early because a change occurred of surgical technique during the study period. The group utilized a pharmacokinetic model from Petroz et al. [1] to estimate target based plasma dexmedetomidine levels. The study the authors based their infusion rates on by Petroz et al. was created in pediatric patients aged 2 yr to 12 yr. The age group in the present study ranged from 10 yr to 25 yr. As pharmacokinetics may differ in a two year old from that of a 25 year old, the question arises as to how reliable the target plasma levels of dexmedetomidine were in the present study. Furthermore, the Petroz study only had 36 patients, far from a robust study to given reliable plasma drugs levels based on a predetermine infusion rate. The plasma levels chosen were 0.4 ng/ml and 0.8 ng/ml for the low and high dex groups respectively. They did the same for propofol. They do not provide us good insight as to what infusion rates were utilized to acheive the target plasma levels cited in the study (i.e. 0.4 ng/ml and 0.8 ng/ml). Although the authors did randomly take plasma samples to verify that the pharmacokinetic model they were using was accurate, there is a small chance that some patients deviated from the target plasma drug level of dex. The small number of patients creates further risk of varying plasma levels disrupting an statistical analysis.
Their study did seem to match the results of two previous studies looking on the effect of dexmedetomidine in neuromonitoring in that SSEPs were not affected at all even at higher dexmedetomidine dosages.[2,3] The previous studies, however, concluded that dexmedetomidine did not effect MEPs in a clinically relevant matter. One of the studies (Bala et al.) utilized two target plasma levels for dex (0.3 ng/ml and 0.6 ng/ml). Once again, one can only wonder if the actual plasma levels of dex in the present study were as claimed. The authors of the current study claim to confirm the results of the other study listed [3], but then state, "...Whereas the other eight patients do not fit into any of our experimental groups as the computed propofol effect site concentration is less than that targeted in our group 2." Tobias looked at 9 patients who received a propofol infusion w/ BIS monitoring. Dexmedetomidine was loaded with a dosage of 1 mcg/kg over 20 minutes. This would provide a plasma concentration per the authors of the present study of 0.84 ng/ml (the same as their high dex group). The first patient in the protocol had a BIS decrement from 58 to 31 indicating overdosage of anesthesia. The protocol in Tobias et al. was then modified to decrease the propofol infusion to maintain a stable BIS as dexmedetomidine was added. Although the MEPs did decrease in the first patient, it was likely a result of very deep anesthesia, and the next eight patients in the Tobias study did not experience a significant decrement in MEPs with dexmedetomidine. The other patients had their BIS maintained at about 50.

i don't agree with the editorial. n schmen. plasma level schmasma level.

they gave clinically relevant doses and there was a marked (not subtle) reduction in mep amplitude. pretty sure your anecdotal n of 100 is the least clinically relevant and least well controlled and statistically worse reason to use dexmed. why risk it? wait for the data....

don't get me wrong - i love dexmed in the right scenes and particularly in peds. i did a LOT of complex pedi spines in fellowship, and i just don't think dexmed is useful in those cases. i'll wait for further data to come out. if you're using dexmed now and a kid comes out with a postop neuro deficit i don't think you can defend yourself on the (lack of) strength of an editorial...

 

[btbam]

Quasi necro-bump here. I'm doing a peds re-do fusion on Monday. They tried about 2 months ago and had decreased motors for most of the case and lost them at some point and decided to abandon. Looking back on the record they did half mac Iso, prop + fent gtts.

Some of the spine surgeons are moving towards TIVA and was wondering what combo you guys would try out for this one... I was thinking prop + dex + fent? Or maybe ketamine instead of prop. Anyone have experience with that combo?

 

[BuzzPhreed]

I don't use Precedex for these cases. It's costly and doesn't really add anything. And it causes a lot of delayed wake ups because people don't know when to turn it off.

I keep it simple. Propofol, fentanyl infusion, and low volatile concentration (like 0.3-0.4 MAC). Never had anyone move, never had anyone remember anything, never had anyone with a palsy after the operation, and never had complaints from the neuromonitoring tech. I shut off the propofol and fentanyl when they are closing and turn up the volatile. As we're rolling them over onto their backs I'm usually pulling the tube. And this technique is the cheapest.

You can add a little ketamine to your propofol (usually 100mg in the first syringe of 50mL of propofol [and none thereafter in subsequent propofol reloads], which gives you 2mg/mL, and run it as a propofol infusion of 50-100mcg/kg/min on your pump asking the tech to periodically monitor for burst suppression [as opposed to surfing on the internet, which is what a lot of them do when the surgeon is not in the spine]). Ketamine increases amplitude and decreases latency in the neuromonitoring. Just make sure you do it up front before baselines are done because it can potentially create false negatives later in the case.

 

[IlDestriero]

Quasi necro-bump here. I'm doing a peds re-do fusion on Monday. They tried about 2 months ago and had decreased motors for most of the case and lost them at some point and decided to abandon. Looking back on the record they did half mac Iso, prop + fent gtts.

Some of the spine surgeons are moving towards TIVA and was wondering what combo you guys would try out for this one... I was thinking prop + dex + fent? Or maybe ketamine instead of prop. Anyone have experience with that combo?

I've always done my spines and cranis with pure TIVA for neuromonitoring, after the mask induction of course.

I do a good number of these a year. My current strategy is: (note-peds cases)
Prop 125-200 (adjusted for BP and rough depth per neuromotoring)
Ketamine 0.1 mg/kg/hr after 1/kg bolus.
Sufenta boluses PRN (1mcg/kg up to 50 q 1-2h based of vitals) stop bolusing when closing. You can do an infusion as well and stop when the rods are in. I used to use Remi which worked fine- 0.1-0.3.
TXA 10/1
Methadone 0.1mg/kg (up to 10) at induction.
Upper and downer of choice as needed. (Neo/nicard)
Keep MAP above 60. Above 70 for correction. If they are losing signals, MAP to 70+ for the whole case.
I don't know why anyone would use volatiles for these cases. When bad things happen it makes it harder to know what is going on. Why have it as a variable at all. I like to keep it simple. If signals drop you can't just switch it off and take it out of the equation. You can just bump the BP, etc in a TIVA and say it's not you, so it is the correction.
I wouldn't use dex for these cases for the same reason as volatiles. Why confuse the picture. It may work great for most cases, but when signals are dropping etc. you've introduced a new and avoidable variable. I might use dex for a tiva for the rare patient where propofol is contraindicated. Dex/high ket/sufenta. Maybe 0.3 MAC of Iso instead of dex. 8)
I'd have to hit the literature for that one.

 

[nimbus]

I don't do kids but for adults I use propofol 1000/ketamine100/remi2 all mixed in 1 vial of propofol. Titrate to BIS and BP, usually 50-100mcg/kg/min of propofol.