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BackgroundPostoperative Delirium (POD) is the most frequent neurocognitive complication after general anesthesia in older patients. The development of POD is associated with prolonged periods of burst suppression activity in the intraoperative electroencephalogram (EEG). The risk to present burst suppression activity depends not only on the age of the patient but is also more frequent during propofol anesthesia as compared to inhalative anesthesia. The aim of our study is to determine, if the risk to develop POD differs depending on the anesthetic agent given and if this correlates with a longer duration of intraoperative burst suppression.MethodsIn this secondary analysis of the SuDoCo trail [ISRCTN 36437985] 1277 patients, older than 60 years undergoing general anesthesia were included. We preprocessed and analyzed the raw EEG files from each patient and evaluated the intraoperative burst suppression duration. In a logistic regression analysis, we assessed the impact of burst suppression duration and anesthetic agent used for maintenance on the risk to develop POD.Results18.7% of patients developed POD. Burst suppression duration was prolonged in POD patients (POD 27.5 min ± 21.3 min vs. NoPOD 21.4 ± 16.2 min, p p = 0.046). Burst suppression duration was prolonged under propofol anesthesia as compared to sevoflurane and desflurane anesthesia (propofol 32.5 ± 20.3 min, sevoflurane 17.1 ± 12.6 min and desflurane 20.1 ± 16.0 min, p p = 0.032).ConclusionWe found a significantly increased risk to develop POD after desflurane anesthesia in older patients, even though burst suppression duration was shorter under desflurane anesthesia as compared to propofol anesthesia. Our finding might help to explain some discrepancies in studies analyzing the impact of burst suppression duration and EEG-guided anesthesia on the risk to develop POD.

BACKGROUNDː Dysglycemia is associated with adverse outcome including increased morbidity and mortality in surgical patients. Acute insulin resistance due to the surgical stress response is seen as a major cause of so-called stress hyperglycemia. However, understanding of factors determining blood glucose (BG) during surgery is limited. Therefore, we investigated risk factors contributing to intraoperative dysglycemia. METHODSː In this subgroup investigation of the BIOCOG study, we analyzed 87 patients of ≥ 65 years with tight intraoperative BG measurement every 20 min during elective surgery. Dysglycemia was defined as at least one intraoperative BG measurement outside the recommended target range of 80-150 mg/dL. Additionally, all postoperative BG measurements in the ICU were obtained. Multivariable logistic regression analysis adjusted for age, sex, American Society of Anesthesiologists (ASA) status, diabetes, type and duration of surgery, minimum Hemoglobin (Hb) and mean intraoperative norepinephrine use was performed to identify risk factors of intraoperative dysglycemia. RESULTSː 46 (52.9%) out of 87 patients developed intraoperative dysglycemia. 31.8% of all intraoperative BG measurements were detected outside the target range. Diabetes [OR 9.263 (95% CI 2.492, 34.433); p=0.001] and duration of surgery [OR 1.005 (1.000, 1.010); p=0.036] were independently associated with the development of intraoperative dysglycemia. Patients who experienced intraoperative dysglycemia had significantly elevated postoperative mean (p

Objective: The benzodiazepine midazolam, a gamma amino butyric acid receptor A (GABAA-) agonist, is frequently administered as premedication before surgery to reduce anxiety and agitation. However, its effects on electroencephalogram (EEG) dynamics at induction of anesthesia with propofol, a GABAA-agonist as well, and during early phases of general anesthesia are still unknown. This study aims to investigate the influence of premedication with midazolam on the pre-operative, frontal EEG and the impact of this GABAA – receptor pre-activation on the intraoperative EEG spectrum after induction of anesthesia with propofol. Methods: Within the framework of this prospective observational trail patients aged ≥ 65 years, undergoing elective surgery were examined. Patients who received premedication with midazolam (Mid, n=15) were compared to patients who did not (noMid, n=30). A continuous pre- and intraoperative frontal EEG was recorded with the Sedline monitor (Masimo). A pooled electrode that equally weighted the signals recorded at the electrode positions Fp1/2 and F7/8 was calculated to obtain estimates of frontal power spectra. Subsequently, absolute power within the delta (0.5-4Hz), theta (4-8Hz), alpha (8-12Hz), and beta (12-25Hz) frequency-bands was analyzed in 10-second EEG-sections before (pre-induction), and after induction of anesthesia with propofol (post-induction), as well as during a stable intraoperative phase of anesthesia that was maintained with either propofol or volatile-anesthetics (intra-operative). Additionally, a “baseline” EEG recorded on the day before surgery, when patients were under no influence of midazolam or propofol, was analyzed in a post hoc approach to validate the results. Results: There was no significant difference in α-power between Mid and noMid patients during the “baseline” EEG recordings. Pre-induction, α-power of Mid patients was lower compared with noMid-patients (α-power: Mid: -10.75 dB vs. noMid: -9.20 dB; p=0.036). After induction of anesthesia Mid-patients displayed a stronger increase of frontal α-power resulting in higher absolute α-power at post-induction state, (α-power: Mid -3.56 dB vs. noMid: -6.69 dB; p=0.004), which remained higher intraoperatively (α-power: Mid: -2.12 dB vs. noMid: -6.10 dB; p=0.024). Conclusion: Midazolam premedication altered the intraoperative EEG-spectrum in elderly patients. Low-dose GABAA activation in form of premedication with midazolam facilitated the activation of frontal α-power in response to induction of anesthesia with propofol. This finding provides further evidence for the role of GABAergic transmission in the appearance of frontal α-power at loss of consciousness and during general anesthesia., Ziel: Das Benzodiazepin Midazolam wird häufig als Prämedikation vor einer Narkose verordnet. Sowohl Midazolam als auch das häufig zur Narkoseeinleitung verwendete Hypnotikum Propofol wirken als GABAA-Agonisten, allerdings an unterschiedlichen Bindungsstellen des Rezeptors. Es wird vermutet, dass GABAA-vermittelte Feedbackmechanismen für einen Anstieg der frontalen -Power im EEG Spektrum unter Vollnarkose verantwortlich sind. Ziel dieser Studie war es zu untersuchen, wie eine Voraktivierung des GABAA-Rezeptors durch Midazolam das EEG Spektrum bei älteren Patienten vor, während, und nach Narkoseeinleitung mit Propofol beeinflusst. Methoden: Im Rahmen dieser prospektiven Beobachtungsstudie wurden Patienten im Alter von ≥ 65 Jahren, die sich einer elektiven Operation mit einer Dauer von mindestens 60 Minuten unterzogen, untersucht. Ein kontinuierliches prä- und intraoperatives frontales EEG wurde mittels des Sedline EEG Monitors (Masimo) bei Patienten, die eine Prämedikation mit Midazolam erhielten (Mid, n = 15), und bei Patienten ohne Prämedikation (noMid, n = 30) aufgezeichnet. Zur Validierung der Ergebnisse wurde zusätzlich ein am Tag vor der Operation aufgezeichnetes „Baseline“ EEG ohne den Einfluss von Midazolam oder Propofol ausgewertet. Für die Auswertung wurden die EEG-Signale der Elektrodenpositionen Fp1/2 und F7/8 gemittelt. Die absolute spektrale Power in den Frequenzbereichen Delta (0,5-4 Hz), Theta (4-8 Hz), Alpha (8-12 Hz) und Beta (12-25 Hz) wurde in 10 Sekunden langen EEG-Abschnitten vor Narkoseeinleitung, nach Narkoseeinleitung mit Propofol sowie während einer stabilen intraoperativen Narkosephase, die entweder mit Propofol oder volatilen Anästhetika aufrechterhalten wurde, untersucht. Ergebnisse: Die α-Power während der Baseline EEGs unterschied sich nicht zwischen beiden Gruppen. Vor Narkoseeinleitung war die α-Power bei prämedizierten Patienten (Mid-Patienten) im Vergleich zu noMid-Patienten deutlich geringer (α-Power: Mid: -10,75 dB vs. noMid: -9,20 dB; p = 0,036). Während der Narkoseeinleitung zeigten Mid-Patienten einen signifikant stärkeren Anstieg der frontalen α-Power, was zu einer höheren absoluten α-Power führte (α-Power: Mid: - 3,56 dB vs. noMid: - 6,69 dB; p = 0,004). Die α-Power blieb auch intraoperativ signifikant höher im Vergleich zu nicht prämedizierten Patienten (α-Power: Mid: -2,12 dB vs. noMid: -6,10 dB; p = 0,024). Zusammenfassung: Eine Prämedikation mit Midazolam verändert das intraoperative EEG-Spektrum bei älteren Patienten. Die Vor-Aktivierung des GABAA-Rezeptors durch Midazolam führt zu einer höheren intraoperativen α-Power nach Propofol-Gabe. Diese Ergebnisse liefern weitere Hinweise darauf, dass der Anstieg der frontalen α-Power während einer Vollnarkose auf GABA-vermittelten Feedback-Mechanismen beruht.

Background: Cognitive abilities decline with aging, leading to a higher risk for the development of postoperative delirium or postoperative neurocognitive disorders after general anesthesia. Since frontal α-band power is known to be highly correlated with cognitive function in general, we hypothesized that preoperative cognitive impairment is associated with lower baseline and intraoperative frontal α-band power in older adults. Methods: Patients aged ≥65 years undergoing elective surgery were included in this prospective observational study. Cognitive function was assessed on the day before surgery using six age-sensitive cognitive tests. Scores on those tests were entered into a principal component analysis to calculate a composite "g score" of global cognitive ability. Patient groups were dichotomized into a lower cognitive group (LC) reaching the lower 1/3 of "g scores" and a normal cognitive group (NC) consisting of the upper 2/3 of "g scores." Continuous pre- and intraoperative frontal electroencephalograms (EEGs) were recorded. EEG spectra were analyzed at baseline, before start of anesthesia medication, and during a stable intraoperative period. Significant differences in band power between the NC and LC groups were computed by using a frequency domain (δ0.5-3 Hz, θ 4-7 Hz, α 8-12 Hz, β 13-30 Hz)-based bootstrapping algorithm. Results: Of 38 included patients (mean age 72 years), 24 patients were in the NC group, and 14 patients had lower cognitive abilities (LC). Intraoperative α-band power was significantly reduced in the LC group compared to the NC group (NC -1.6 [-4.48/1.17] dB vs. LC -6.0 [-9.02/-2.64] dB), and intraoperative α-band power was positively correlated with "g score" (Spearman correlation: r = 0.381; p = 0.018). Baseline EEG power did not show any associations with "g." Conclusions: Preoperative cognitive impairment in older adults is associated with intraoperative absolute frontal α-band power, but not baseline α-band power., Seventh Framework Programme (European Commission) (FP7/2007-2013) (Grant HEALTH-F2-2014-60246)

BACKGROUNDː Dysglycemia is associated with adverse outcome including increased morbidity and mortality in surgical patients. Acute insulin resistance due to the surgical stress response is seen as a major cause of so-called stress hyperglycemia. However, understanding of factors determining blood glucose (BG) during surgery is limited. Therefore, we investigated risk factors contributing to intraoperative dysglycemia. METHODSː In this subgroup investigation of the BIOCOG study, we analyzed 87 patients of ≥ 65 years with tight intraoperative BG measurement every 20 min during elective surgery. Dysglycemia was defined as at least one intraoperative BG measurement outside the recommended target range of 80-150 mg/dL. Additionally, all postoperative BG measurements in the ICU were obtained. Multivariable logistic regression analysis adjusted for age, sex, American Society of Anesthesiologists (ASA) status, diabetes, type and duration of surgery, minimum Hemoglobin (Hb) and mean intraoperative norepinephrine use was performed to identify risk factors of intraoperative dysglycemia. RESULTSː 46 (52.9%) out of 87 patients developed intraoperative dysglycemia. 31.8% of all intraoperative BG measurements were detected outside the target range. Diabetes [OR 9.263 (95% CI 2.492, 34.433); p=0.001] and duration of surgery [OR 1.005 (1.000, 1.010); p=0.036] were independently associated with the development of intraoperative dysglycemia. Patients who experienced intraoperative dysglycemia had significantly elevated postoperative mean (p