Speaker: Chris Martin, Surgical Neurophysiologist (6:09) speaks at TxANA Conference Part IV
In August, 2016, Neuro Alert exhibited at the TxANA Annual Convention & Trade Show. Here, Chris Martin, one of Neuro Alert’s Senior Surgical Neurophysiologists, was asked to present “Introduction to Intraoperative Neurophysiology” and “Intraoperative Monitoring Applications and Considerations.” In this six-part presentation, Martin walks us through the origins of Intraoperative Monitoring to present-day applications.
Transcripts to follow:
Chris Martin, CNIM, Surgical Neurophysiologist:
I want to talk about some case reports of changes that we caught that get into why we’re there, but, also almost in every case, changes that could have been caused by anesthetic drugs or by something iatrogenic that the surgeon has done. It’s really up to us to suss that out and figure out which is which.
For the first one, it’s a carotid endarterectomy, this is a standard history of this patient here. The interesting, I guess, notable thing in this case was that the right carotid was giving a lot of posterior circulation supply because the two verts were also stenosed. Left sides was 89% stenosed as well, but they decided to use the right carotid since it was also contributing to this posterior circulation via a large posterior cerebral artery. Here you can see the bilateral stenosis, really the left looks worse than the right here, but there’s the lesions there on the right, the left carotids.
Anesthesia used includes: a neuromuscular block, a Mac and a half of sevo, and 50% nitrous. Every one of my neuro monitoring friends might be horrified by that, but that’s perfectly accepted. I’m not going to stand here and be dogmatic and say, “You need to do TIVA for every single case.” It depends on what the surgery is. In this case it’s a carotid. We’re not doing sensory evoked potentials necessarily. We’re not doing motor evoked potentials. We’re not doing EMG. Neuromuscular block is perfectly fine, and in fact, I prefer it because muscle tone is a source of noise from the EEG signal that we’re trying to record, as you see. If we can eliminate that right off the block and throughout the case, that’s great.
Same with one and a half mac of sevo and some nitrous. If we get a good continuous EEG under a regiment like this then that’s great – as long as that’s how it stays and you reach steady state and you don’t give any boluses right when they’re heparinized and knock the brain out altogether. We can work together to make it as collaborative as possible in the management anesthetically of the patient. We don’t have to just say, “We require this,” or, “We require that.”
Here’s what the baseline looked like: left hemisphere over right hemisphere. Here’s the anesthesia. The mean was 82, that’s a good number. It’s nice and symmetric, a typical picture of someone under general anesthesia. There’s some sort of theta, alpha and theta frequency activity, some underlying beta and a little bit of delta slow waves as well. This is a good patient. They’re not about to wake up. It’s nice and symmetric and we have some good continuity as well. Again, pre-clamp, so we’re just making sure that we’re in continuous EEG. We’re not in burst suppression, and everything is ready to go right before the surgeon clamps. Maybe the means bumped a little bit, everything is all set.
20 seconds after the clamp goes on the right carotid here’s what we see. It’s gotten slower in general bilaterally. There’s just more theta and delta activity, but you can also appreciate that the amplitude on the right hemisphere is lower than it is on the left hemisphere. We have unilateral decrease in amplitude and we have bilateral slowing. There’s just less fast frequency activity.
We recommended at that point that, again, here’s just the anesthesia has stayed stable. This change is persisting now 20 seconds post clamp. The surgeon now places a shunt. That’s our recommended intervention in the event of a change like that with clamping. This is now 10 seconds after the shunt’s placed. We’re still seeing a slower EEG than it was at baseline prior to clamping. There’s still generalized global delta on both sides, both hemispheres.
Now we’re at two minutes 15 seconds post shunt, it looks a lot better. The fast frequency stuff is back. The amplitude on the right side is back, so it looks almost spec to baseline. The symmetry is back so the shunt seems to have effectively helped reprofuse the area of brain that was becoming ischemic. When you take the shunt out you have to reclamp again and we saw the same changes. You can see still that it’s unilaterally lower in amplitude on the right side, but bilaterally slower. They took the clamp off to finish the closure and it came back.
By the end of the case with a mean of 91, the EEG was symmetric, good fast activity, and that’s fine. This is that same sort of series of changes displayed over a spectral analysis array where the power of each frequency is displayed in these various colors. You can see everything is chugging along, clamp goes on here, and then everything dive bombs down here, so it’s all washed out. It gradually returns back to the baseline with the shunt placement. That’s a good catch of a potential stroke that would’ve happened if we hadn’t detected that.
Here’s the postop images. The right side is nice and patent now and big lumen and then the left side still has a stenosis probably needs to be done.