• Juan C Pedemonte, George S Plummer, Shubham Chamadia, Joseph J Locascio, Eunice Hahm, Breanna Ethridge, Jacob Gitlin, Reine Ibala, Jennifer Mekonnen, Katia M Colon, M Brandon Westover, David A D'Alessandro, George Tolis, Timothy Houle, Kenneth T Shelton, Jason Qu, and Oluwaseun Akeju.
• From the Departments of Anesthesia, Critical Care, and Pain Medicine (J.C.P., G.S.P., S.C., E.H., B.E., J.G., R.I., J.M., K.M.C., T.H., K.T.S., J.Q., O.A.) Department of Neurology (J.J.L., M.B.W.) Department of Surgery, Division of Cardiac Surgery (D.A.D., G.T.) Henry and Allison McCance Center for Brain Health (M.B.W., O.A.) Clinical Data Animation Center (M.B.W.), Massachusetts General Hospital, Boston, Massachusetts Department of Anesthesiology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile (J.C.P.) Tufts University School of Medicine, Boston, Massachusetts (G.S.P.).
• Anesthesiology. 2020 Aug 1; 133 (2): 280-292.

BackgroundIntraoperative burst-suppression is associated with postoperative delirium. Whether this association is causal remains unclear. Therefore, the authors investigated whether burst-suppression during cardiopulmonary bypass (CPB) mediates the effects of known delirium risk factors on postoperative delirium.MethodsThis was a retrospective cohort observational substudy of the Minimizing ICU [intensive care unit] Neurological Dysfunction with Dexmedetomidine-induced Sleep (MINDDS) trial. The authors analyzed data from patients more than 60 yr old undergoing cardiac surgery (n = 159). Univariate and multivariable regression analyses were performed to assess for associations and enable causal inference. Delirium risk factors were evaluated using the abbreviated Montreal Cognitive Assessment and Patient-Reported Outcomes Measurement Information System questionnaires for applied cognition, physical function, global health, sleep, and pain. The authors also analyzed electroencephalogram data (n = 141).ResultsThe incidence of delirium in patients with CPB burst-suppression was 25% (15 of 60) compared with 6% (5 of 81) in patients without CPB burst-suppression. In univariate analyses, age (odds ratio, 1.08 [95% CI, 1.03 to 1.14]; P = 0.002), lowest CPB temperature (odds ratio, 0.79 [0.66 to 0.94]; P = 0.010), alpha power (odds ratio, 0.65 [0.54 to 0.80]; P < 0.001), and physical function (odds ratio, 0.95 [0.91 to 0.98]; P = 0.007) were associated with CPB burst-suppression. In separate univariate analyses, age (odds ratio, 1.09 [1.02 to 1.16]; P = 0.009), abbreviated Montreal Cognitive Assessment (odds ratio, 0.80 [0.66 to 0.97]; P = 0.024), alpha power (odds ratio, 0.75 [0.59 to 0.96]; P = 0.025), and CPB burst-suppression (odds ratio, 3.79 [1.5 to 9.6]; P = 0.005) were associated with delirium. However, only physical function (odds ratio, 0.96 [0.91 to 0.99]; P = 0.044), lowest CPB temperature (odds ratio, 0.73 [0.58 to 0.88]; P = 0.003), and electroencephalogram alpha power (odds ratio, 0.61 [0.47 to 0.76]; P < 0.001) were retained as predictors in the burst-suppression multivariable model. Burst-suppression (odds ratio, 4.1 [1.5 to 13.7]; P = 0.012) and age (odds ratio, 1.07 [0.99 to 1.15]; P = 0.090) were retained as predictors in the delirium multivariable model. Delirium was associated with decreased electroencephalogram power from 6.8 to 24.4 Hertz.ConclusionsThe inference from the present study is that CPB burst-suppression mediates the effects of physical function, lowest CPB temperature, and electroencephalogram alpha power on delirium.

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