The nuts and bolts of multimodal anaesthesia in the 21st century: a primer for clinicians

Abstract

Purpose of review: This review article explores the application of multimodal anaesthesia in general anaesthesia, particularly in conjunction with locoregional anaesthesia, specifically focusing on the importance of EEG monitoring. We provide an evidence-based guide for implementing multimodal anaesthesia, encompassing drug combinations, dosages, and EEG monitoring techniques, to ensure reliable intraoperative anaesthesia while minimizing adverse effects and improving patient outcomes.

Recent findings: Opioid-free and multimodal general anaesthesia have significantly reduced opioid addiction and chronic postoperative pain. However, the evidence supporting the effectiveness of these approaches is limited. This review attempts to integrate research from broader neuroscientific fields to generate new clinical hypotheses. It discusses the correlation between high-dose intraoperative opioids and increased postoperative opioid consumption and their impact on pain indices and readmission rates. Additionally, it explores the relationship between multimodal anaesthesia and pain processing models and investigates the potential effects of nonpharmacological interventions on preoperative anxiety and postoperative pain.

Summary: The integration of EEG monitoring is crucial for guiding adequate multimodal anaesthesia and preventing excessive anaesthesia dosing. Furthermore, the review investigates the impact of combining regional and opioid-sparing general anaesthesia on perioperative EEG readings and anaesthetic depth. The findings have significant implications for clinical practice in optimizing multimodal anaesthesia techniques (Supplementary Digital Content 1: Video Abstract, http://links.lww.com/COAN/A96 ).

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FIGURE 1

The interplay of preoperative risk factors and postoperative pain. A simplified chart illustrating the connection between postoperative pain, preoperative anxiety, and other risk factors like sleep disorders or smoking. Risk factors influence and intensify each other, are potentiated by certain intraoperative actions, influencing pain and its chronification, sleep patterns, and cognitive recovery, in a vicious cycle.

FIGURE 2

Nonpharmacological interventions in analgesia and anxiolysis: clinicians are increasingly employing nonpharmacological therapies for preoperative anxiety. A caring relationship releases endogenous opiates in patients as outlined in Jaak Panksepps's ‘brain opioid hypothesis of social relations’ [57]. This moderates adrenergic stress reactions, engaging mu-receptors for further pain reduction [58^▪]. ‘Mind–body therapies’ (hypnosis, meditation, cognitive–behavioural therapy, guided imagery, etc.) can positively influence anxiety, nociception, and opiate consumption [48]. Music [52,54], a computer game, or a film can be added to pharmacological premedication as distractive elements, especially with children. ‘Music-induced analgesia’ [59] can be explicitly used as premedication, as confirmed in a meta-analysis including 4968 patients from 55 studies, where the use of midazolam, opiates, and propofol was significantly reduced.

FIGURE 3

Multimodal analgesia bundle. Schematic representation of multimodal anaesthesia divided according to premedication, induction, maintenance, and postoperative analgesia in chronological sequence. This bundle can also be used with sevoflurane as the primary anaesthetic. MMA's main principle states that pharmacological analgesia synergistically inhibits nociception and arousal. For this reason, the primary anaesthetic must be reduced during maintenance based on the EEG signal.

FIGURE 4

Case vignette of a frontal EEG during multimodal anaesthesia: representation of frontal EEG in a multitaper spectrogram. The black dots reflect spindle density and were detected by an automatic spindle detection program (YASA, Yet Another Spindle Algorithm) [120]. After a dexmedetomidine bolus, induction was undertaken with propofol and alfentanil, resulting in delta-dominant anaesthesia with few spindles (grey arrow). After emerging from burst suppression, spindle-rich anaesthesia (8–12 Hz) with high delta (0–4 Hz) power ensues. Administering a ketamine bolus (red arrow) adds power in the beta frequency range and elevates the spindles’ frequency to 13–15 Hz for about 15 min. At the same time, a decrease in delta power (blue arrow) can also be observed. A lidocaine bolus of 0.5 mg/kg was administered during the application of the sub-Tenon block (lower green arrow): the EEG shows a short-term synchronous increase in delta waves, a temporary reduction in spindle density and an eye-muscle artefact because of the application of the eye block (upper green arrow). BD, beta-dominant GA; DD, delta-dominant GA; EM, emergence period; SD, spindle-dominant GA; W, wakefulness.