It has been almost a year since the PAAD discussed desert island monitors. What’s a desert island monitor? Basically, if you were stranded on a desert island and could have only one anesthesia monitor what would it be? The obvious choices have been pulse oximetry and/or capnography. Perhaps another is a quantitative neuromuscular blockade monitor. Over the next 2-3 weeks we’ll be reviewing several papers on the use of intraoperative EEG monitoring to guide anesthetic vapor and propofol delivery, as our new desert island monitor. Indeed, I was quite literally blown away by these papers and I think you will be too.
When working with residents and young (well everyone is young compared to me) faculty and talking about the days before pulse oximetry and capnography, I would always get this look of disbelief. “How could you possibly have provided anesthesia without those monitors”? I think 5-10 years from now, you will get the same look when talking about the provision of anesthesia without EEG. Because this is such a big deal, I am going to start with a relatively recent primer article and then move forward to more current papers. Additionally, I’ve asked Drs. Ian Yuan and Dean Kurth from the Children’s Hospital of Philadelphia, the first and last authors of these papers, to assist me in these reviews. Myron Yaster MDReview article
Ian Yuan, Ting Xu, Charles Dean Kurth. Using Electroencephalography (EEG) to Guide Propofol and Sevoflurane Dosing in Pediatric Anesthesia. Anesthesiol Clin. 2020 Sep;38(3):709-725. PMID: 32792193
Although sevoflurane has been the primary anesthetic drug used in pediatric practice for the last 30+ years, TIVA with propofol has not only gained in popularity but may exceed sevoflurane use in the coming years. Why? Propofol is associated with a lower incidence of laryngospasm, airway obstruction, emergence agitation, and post-operative nausea and vomiting and perhaps most importantly a lower carbon footprint for greenhouse gas emissions. In perhaps all of the world except the United States, “propofol is administered by target-controlled infusion pumps, which deliver propofol based on population derived pharmacokinetic models of volume of distribution and clearance for the target effect site concentration (Ce) of propofol in the brain”.1, 2
Although we don’t often think of it this way, “sevoflurane dosing is also based on clinical parameters, pharmacokinetic models based on uptake and distribution and MAC, as well as monitoring of alveolar end-tidal concentration, which serves as a biomarker for sevoflurane Ce in the brain. Unlike sevoflurane, there is no practical way to monitor the Ce of propofol. This can result in under- or over-dosing of propofol, particularly common in infants and young children due to biological variations in pharmacokinetics and pharmacodynamics related to age, as well as differences in body water/fat composition, kidney and liver function, and brain maturity”.1-3 So in the United States, how do we dose propofol infusions in clinical practice. We basically guess and rely on autonomic responses to surgical stimulation, which has more to do with pain than consciousness!
Is there a better way? Yes, continuous EEG monitoring! So, this is NOT your father’s EEG like the BIS monitor! Before discussing how we can implement this technology of lots of complex squiggly lines into our practices, in today’s PAAD we are going to offer a very, very brief primer which will be the basis for forthcoming PAADs on this subject. As an absolute novice, I (MY) would also recommend a series of 6 short Youtube videos (
), each about 5 minutes, on this subject from the IARS as you get started. In future PAADs we’ll discuss how Ian and Dean implemented a teaching program at CHOP to get the anesthesia care team members on board.2 Finally, I believe that this subject will be presented at an upcoming SPA meeting in the near future.
“Intraoperative EEG monitors typically combine 4 to 8 electrodes into a disposable sensor placed on the forehead. Intraoperative EEG monitors approved for pediatric use include BIS (Medtronic, Minnesota, Minnesota), Narcotrend (MonitorTechnik, Bad Bramstedt, Germany), and SedLine (Masimo, Irvine, California). EEG waveforms are described using amplitude (how much the wave moves up and down) and frequency (how fast the wave moves up and down). Slow (<1hz) and delta waves (1-4hz) with large amplitudes are seen in deep sleep or coma, whereas theta waves (4-7hz) are present in light sleep. Alpha waves (8-12hz) are seen in an awake state with eyes closed or when meditating, whereas faster beta waves (13-30hz) are present in a state of active thinking”.1 How can you tell which is which? Actually by color.
“The decomposition of an EEG waveform into discrete frequency bands (e.g. slow, delta, theta, alpha, beta, and gamma) over time allows creation of a spectrogram also known as a density spectral array (DSA), a type of processed non-proprietary EEG parameter (figure). The DSA displays the relationship between EEG power and frequency over time. In the DSA, the x-axis represents time and y-axis represents frequency. To display EEG amplitude/power at a certain frequency and time, a colored or grey scale is used to represent power intensity, with dark-brilliant colors representing higher power and light-dull colors denoting lower power. The figure below illustrates an example of DSA during 30 minutes of a propofol anesthetic. At minutes 0-5, the majority of EEG power is concentrated in lower frequencies, denoted by the intense red color at frequencies < 3 Hz (lower left), while a minority of EEG power exists in higher frequencies, denoted by blue color at frequencies > 15 Hz. At minutes 8-27, there is an increase in power at frequencies 10-12 Hz as indicated by the appearance of yellow/orange colors, along with a decrease in power at frequencies < 5 Hz as indicated by the change from red to yellow. The DSA shows that the level of hypnosis was greater at minutes 0-5 than at 8-27, as indicated by the majority of power existing in lower frequencies in minutes 0-5. Because propofol and sevoflurane exert dose-dependent effects on frequency and power, the DSA can visually display hypnotic level during the course of the anesthetic.”1
The reason to use non-proprietary EEG parameters is that proprietary processed EEGs like the BIS may be inaccurate in different age groups and with different anesthetic agents. For example, the BIS index may be accurate for GABA A agents like propofol but are completely inaccurate for drugs that are NMDA based agents like ketamine. On the other hand, unprocessed raw EEG combined with non-proprietary processed EEG parameters are reliable biomarkers of propofol and sevoflurane levels across all ages and can be used as a biomarker of hypnotic depth in neonates, infants, and children to guide the dosing of propofol and sevoflurane in individual patients, rather than on population pharmacokinetics.
In the next few PAADs we will review articles on how to implement EEG into practice, how EEG can be used to avoid anesthetics that are too deep (basically isoelectric EEGs), and how EEG can be used to guide anesthetic dosing at different parts of a case (induction, maintenance and emergence). So in the immortal word of Bette Davis: