Introduction

Whether electroencephalography (EEG) can lead to lower rates of postoperative neurocognitive disorders is still a topic of debate (1, 2). However, there are very strong indications for processed EEG (pEEG), which were addressed by the APSF in a 2022 publication (3).  The APSF suggests that patients who are receiving less than 0.7 MAC of inhaled anesthetic  or total intravenous anesthesia (TIVA) when combined with a neuromuscular blocker should have pEEG utilized as an additional intraoperative monitor. The authors also note that “in some patients, it is not possible to maintain an inhaled anesthetic concentration consistent with 0.7 MAC due to hemodynamic compromise, and in those patients, monitoring for the risk of awareness is especially compelling.” This statement brings into light another extremely valuable benefit, that is titrating down your hypnotic under EEG guidance to reduce pressor use and  promote hemodynamic stability.

Case Presentation

Our patient is a 79-year-old man with past medical history significant for coronary artery disease (CAD), chronic obstructive pulmonary disease (COPD), end-stage renal disease (ESRD) on dialysis, seizures, heart failure with preserved ejection fraction, hypertension, and cognitive impairment, who presented with left lower extremity weakness and gait instability for about 3 weeks.  The cervical magnetic resonance imaging (MRI) showed moderate and severe stenosis at C3-6 with an associated T2 signal change. The patient did not tolerate induction of anesthesia leading to severe hemodynamic instability, case cancelation and cardiology consultation.  Several days later, after cardiology clearance, the case was successfully initiated (central line and arterial lines placed). SSEP and MEP monitoring were being utilized, leading to a mixed IV anesthetic and inhalational anesthetic technique with no neuromuscular blockade. Eventually, a transition of care was completed between attendings.

On handoff, the employed anesthetic technique included Sevoflurane I/E 0.9/0.8%, propofol 75 mcg/kg/min and remifentanil 0.05 mcg/kg/min. He was on norepinephrine 0.04 mcg/kg/min and vasopressin 0.02 mcg/min drips. A 4-channel frontal bilateral EEG sensor was placed by the receiving attending, generating this output (Fig 1).

Figure 1. Amplitude resolution set at 3 µV/mm and power bar set at 0/-40 to augment the EEG signal and power. Profound burst suppression (BS) was quantified between 40-54% by the monitor’s algorithm. Burst Suppression (BS) can be seen on raw EEG as an alternating flat period followed by a suppressed burst. The density spectral array (DSA) demonstrates frequent black fill (with blue tips) representing BS on this specific manufacturer’s monitor.

Over about 20 minutes, Sevoflurane was decreased to I/E 0.4/0.4% resulting in more periods of continuous EEG (Fig 2). At that time, neurosurgery notified the anesthesia team that closure was being initiated, after which propofol was discontinued and hypnotic changed to inspired Sevofluane 1%.  The EEG tracing then became continuous prior to emergence (Fig 2). All pressors were titrated to off within 15 minutes and well before emergence.

Figure 2. As hypnotic (sevoflurane) was down-titrated over 15-20 minutes, more periods of continuous EEG were appreciated. As closure was initiated, propofol was discontinued and sevoflurane reverted back to 1% inspired. EEG became continuous prior to emergence (panel 3).

Discussion

This case illustrates many important considerations. During the first surgery, the degree of intraoperative hemodynamic compromise following induction of anesthesia was so significant as to necessitate intraoperative cancellation, a fairly rare occurrence. This prompted close evaluation and preparation for the second attempt at cervical decompression, preceded by a pre-induction arterial line. The patient did develop hypotension again but he stabilized on a mix of hypnotics and vasopressors.

The patient’s comorbidities, including the history of hypertension, CAD and heart failure argues for a higher mean arterial pressure (MAP) goal (greater than 65 mm Hg), not only to avoid end organ damage but also to satisfy neurosurgical preferences in the setting of spinal cord compression (4).  Given these factors, every effort should be made to optimize hemodynamics, including the limitation of hypnotic dose which is known to contribute to hypotension. Although mostly anecdotal, it is not unusual for EEG-guided hypnotic drug administration to prevent hemodynamic instability and pressor use. A recent randomized controlled trial (RCT) (6) reported that a significantly lower dose of norepinephrine was needed to maintain a MAP above 65 mm Hg in vascular surgery patients monitored with pEEG. In this study, practitioners relied on the index value displayed by the device, as well as the 95% spectral edge frequency.

Advanced age with cognitive impairment, and multiple other risk factors also place this patient at an elevated risk for the development of postoperative neurocognitive disorders (5). While burst suppression is sometimes intentionally induced for protection of the brain against ischemia during high-risk surgical procedures as it decreases the brain’s metabolic demand (7), there are theoretical reasons that it can be harmful to neurons (8). Intraoperative pEEG facilitates personalized drug dosage to help achieve anesthetic goals by taking into account age, brain health (and its reserve), and patient factors that impact the central nervous system (i.e. co-existing disease, prescription and illicit drugs).

In summary, pEEG  (with the avoidance of burst suppression and optimization of other easily applied pEEG parameters) is a common-sense monitoring modality which permits targeted hypnotic titration while preventing the hemodynamic consequences of its overdose. An anesthetic technique that limits hypnosis (and minimizes time in burst suppression) may also minimize the anesthesia-associated risk of postoperative neurocognitive disorders. Processed EEG, at minimum, facilitates the integration of personalized anesthetic titration.

References:

1. Byrne K, Grivas M, Gaskell A. ENGAGES-Canada: Has This “Burst” the Bubble of Processed EEG? J Cardiothorac Vasc Anesth. 2024 Dec;38(12):2882-2884
2. Reese M, Wright MC, Roberts KC. et al. Associations between anesthetic dose-adjusted intraoperative EEG alpha power, processing speed, and postoperative delirium: analysis of data from three prospective studies. Br J Anesth. 2025;135(1):109-120
3. The APSF Committee on Technology. APSF-endorsed statement on revising recommendations for patient monitoring during anesthesia. APSF Newsletter. 2022;37(1):7–8.
4. Tetreault LA, Kwon BK, Evaniew N et al. A Clinical Practice Guideline on the Timing of Surgical Decompression and hemodynamic Management of Acute Spinal Cord Injury and the Prevention, Diagnosis, and Management of Intraoperative Spinal Cord Injury: Introduction, Rationale, and Scope. Global Spine Journal 2024 Mar;14(3_suppl):10S-24S
5. Evered LA, Sibert BS. Postoperative Cognitive Dysfunction and Noncardiac Surgery. Anesth Analg 2018;127:496-505
6. Thomsen KT, Sessler DI, Krause L. et al. Processed Electroencephalography-guided General Anesthesia and Norepinephrine Requirements: A randomized trial in Patients Having Vascular Surgery. J Clin Anesth. 2024 Aug:95:111459
7. Siddiqui AZ, Froese L, Gomez A et al. The Effect of Burst Suppression on Cerebral Blood Flow and Autoregulation: a Scoping Review of the Human and Animal Literature. Front Physiol. 2023 Jun 7;14:1204874
8. Pawar N, Barreto Chang OL. Burst Suppression During General Anesthesia and Postoperative Outcomes: Mini Review. Front. Syst. Neurosci. 2022;15:767489