The study was approved by the Ethics Committee of Tohoku University School of Medicine (No. 21334). The written informed consent was obtained from the patient for publication of this case report and any accompanying images. A 52-year-old male (180 cm, 84.2 kg) suffered from septic shock due to right femur necrotizing fasciitis. He had no history of epilepsy or head injury. Preoperative brain computed tomography and chest X-ray revealed no abnormalities. Electrocardiogram (ECG) showed a normal sinus rhythm. Five days after the initial operation of the right below-knee amputation, debridement was planned for local infection control. He was classified as American Society of Anesthesiologists (ASA) Physical Status Class 3E.
Under intravenous sedation with dexmedetomidine (12 μg h−1) and fentanyl (100 μg h−1), the patient successfully adapted to a mechanical ventilator with endotracheal intubation. Besides standard ASA monitoring, invasive blood pressure was continuously recorded by an automated anesthesia recording system (PRM-7000; Nihon Kohden Co., Tokyo, Japan). The DOA was evaluated with Root® with SedLine® Brain Function Monitoring Version 1.8.1.4i (Masimo Inc, Irvine, CA), as a standalone monitor. Surgical anesthesia was induced with additional propofol (500 mg h−1), remifentanil (1 mg h−1), and rocuronium (50 mg). Continuous infusion of phenylephrine (1 mg h−1) controlled the intraoperative hemodynamics while maintaining his mean arterial pressure within 25% of the baseline value (i.e., hypotension-related EEG abnormalities were minimized). His heart rate was stable at around 64 bpm without arrhythmia. The EEG showed a rhythmic, heart rate time-locked pulsation artifact over one of four traces, L2, when there was a momentary pause in the electrocautery interferences (Fig. 1a). Arterial pulsation was palpable beneath the L2 electrode. The electrode impedance and cable connection were checked, and the pulse wave-like artifact diminished after repositioning the L2 electrode. Thereafter, all four traces showed the same EEG pattern as the burst-suppression (Fig. 1b). The PSi, a DOA index calculated by SedLine® Brain Function Monitoring, did not remarkably change. No electrolyte imbalance or hypoglycemia (195 mg dL−1) was observed. Arterial blood gas analysis showed an acceptable level of oxygenation. Four days after the second operation, a full recovery, without neurological deficits, was confirmed following extubation.
Numerical values recorded by PRM-7000 and EEG data were exported from SedLine® using the European Data Format and analyzed offline using MATLAB (Mathworks, Natick, MA, USA). Details of the four EEG channels, ECG, and plethysmography before and after the electrode replacement are shown for two 10-s samples (left and right images) in Fig. 1c. To show time locking between the slow-wave EEG and ECG, the EEG signal was first filtered using a linear-phase low-pass filter (cut-off frequency 1.5 Hz), then the Hilbert transform was applied to obtain the analytic signal and the instantaneous frequency was expressed as the digital derivative of the phase of the analytic signal. Finally, the instantaneous frequency curve was smoothed using a moving average over a 4-s window. The instantaneous frequency of the low-frequency component of L2 coincided with the heart rate due to the pulsation artifact and was separated after electrode replacement (Fig. 1d).