Intraoperative EEG For Depth Of Anesthesia?

There seems to be some confusion on the effectiveness of intraoperative EEG being able to determine some sort of depth of anesthesia. We seem to find ourselves in this scenario far too often where anesthesia asks us...

“My blood pressure just jumped. Can you look at your EEG and tell me if the patient is getting light?”

What Does Depth Of Anesthesia Mean?

The depth of anesthesia?refers to?the degree to which the central nervous system (CNS) is depressed. This should encompass the patient’s chances of being alert, the patient’s chance of remembering something, and/or the patient’s chances of moving to a noxious stimulus.

Some levels are outlined when looking at the depth of anesthesia:

Level 1: baseline recording: awake (premedicated);

Level 2: patient is sedated, but responsive to the calling of his/her name

Level 3: visible motoric responses, either spontaneous or to a noxious?stimulus, but no response to the calling of a name

Level 4: no visible motoric responses, but autonomous responses?still present, either spontaneous or to noxious stimuli

Level 5: no visible motoric or autonomous responses present.

But that is not what is typically being asked of us in the middle of the case. Because we ask anesthesia to allow for movement in many of our cases, they become concerned with patient movement during the case (understandable). So when they ask us if the patient is getting light, they might be asking “is the patient about to move?” That’s level 3, which is deeper than responsiveness.

In fact, when looking at the best way to assess patient awareness is by identifying patient movement.

Right off the bat, a movement to a painful event is reflexogenic in nature. While there is central modulation over the spinal cord from the cortex, it is more than a stretch to think that intraoperative EEG recordings can be used to monitor spinal cord excitability. So there is no way that we can take a look at our EEG and say…

“Nope, that patient isn’t going to react to pain at all.”

So we aren’t in the best position to start.

But what about using EEG to better assess patient awareness or wakefulness?

It has been well documented that initial doses of an inhalational agent will cause a desynchronization and acceleration of EEG patterns that will slow and increase in amplitude as the dose is increased. Intraoperative EEG patterns with inhalational agents look like this:

Use of these?patterns has been associated with a patient becoming “light” or “deep,” however; there are no criteria that are sensitive or specific for predicting awareness, memory, or movement.

To complicate it even further, the real-world transition from one pattern to the next is not a smooth curve like the image depicts. Other factors can create even more difficulty in interpreting the waveforms and assigning a depth of anesthesia to the patterns generated.

• Intraoperative EEG patterns can often jump levels. And this jumping of levels can be to due to either higher doses of inhalational agents administered or a combination of some other drugs.
• Not all drugs have similar patterns.?Ketamine and NMDA antagonists (e.g., nitrous oxide) do not produce the typical EEG changes that are seen during general anesthesia.
• Various pathophysiological events also affect the EEG (e.g. hypotension, hypoxia, hypercarbia). Such events may modify both the patient’s level of consciousness and the expected EEG signature that any given anesthetic agent generates, thus confounding interpretation.

Studies have looked at spectral edge frequency with isoflurane and propofol, as well as processed?EEG using isoflurane. Same thing in a?second study. They all came to the same conclusion: EEG is not sensitive or specific for determining the depth of anesthesia.

What sticks out is that those were in favorable conditions, and there wasn’t a mixing of different medications. For instance, opioid analgesics or a combination of agents can cause burst suppression to disappear. Adding a mixed cocktail can also cause an absence in one or more intraoperative EEG patterns or changes in the occurrence of slow wave patterns.

Some facilities might have more strict anesthetic protocols, but the ones I am used to working at vary depending on the provider and patient presentation.

So far I’ve only shown concern for making sure that the patient doesn’t get “light,” but we need to be concerned with the other side of the coin. We should also be cautious when asking anesthesia?to increase the amount of agent simply by looking at intraoperative EEG recordings. Placing a patient deeper than necessary is associated with a longer recovery that is also less tolerable. Deep anesthesia brings concerns about other postoperative complications, like mortality, delirium, cognitive decline, dementia, myocardial infarction, stroke, renal failure, and cancer (controversial).

But ask an IONM clinician about how they see EEG, they might respond:

“Oh, but I only use depth of anesthesia to make sense of my SSEP and MEP”

Using EEG To Quantify SSEP and MEP

This seems to be the more common use of intraoperative EEG for “depth of anesthesia.”

Before I get into it, I just want to offer up a bit of a warning on documentation. Because the terminology “depth of anesthesia” originated and is owned by anesthesia assessing the patient’s state under anesthesia, I would try to steer clear of using that same terminology to discuss the assessment of evoked responses under anesthesia. Maybe I’m being a little overcautious here, but I can easily see this being taken out of context. An opposing attorney might say:

“The patient moved during the procedure and sustained injuries. According to your notes, you were monitoring the depth of anesthesia. Why did you not alert the surgeon that the patient was getting light leading up to them moving?”

It seems like there is a different/better way to discuss and document the use of intraoperative EEG for depth of anesthesia as it relates to your SSEP and MEPs that won’t leave you exposed to something out of your scope of practice that you can’t accurately monitor.

But let’s get back on track here…

Using Intraoperative EEG To Quantify SSEP and MEP

I understand the concept that if EEGs are showing signs of slowing or even moments with isoelectric readings the brain is metabolically less active. We might also be able to assume that synapses that do not even necessarily reside in the cortex?will also be affected by anesthesia and can cause even greater effects on SSEP and MEP recordings.

Where I am having trouble is trying to quantify it to make it useful. I would assume that all the other variables that make intraoperative EEGs difficult/impossible to use to determine the?depth of anesthesia would also factor in what we might see in our potentials. Probably even more difficult, because the motor and sensory pathways synapse multiple times in areas distant to the cerebral?cortex.

But maybe I’m not describing the context of its usefulness like others might… just a roundabout guess that could possibly explain why global amplitudes increased or decreased in size or morphology from one point in time to the next. Nothing to hang your hat on, you might be wrong almost as much as you might be right and it means nothing without trying to compare it to other findings throughout the case.

Or am I wrong here? Is there a way to use it with some accuracy? I’d like to get to the bottom of what’s being taught and accepted out in the field.

[PS – if you’re for using it and find it helpful, please explain how you use it. “It works for me!” doesn’t work for me as a good explanation.]