2157 – Cortisol levels and neuropsychiatric diagnosis as markers of postoperative delirium

Abstract

IntroductionDelirium affects 11% to 47% of post-operative cardiac surgery patients and is associated with higher mortality and morbidity rates. However, the pathophysiology of this syndrome is largely unknown.ObjectivesTo investigate whether increased concentration of pre- and postoperative plasma cortisol predicts the development of delirium after coronary artery bypass graft surgery (CABG). Secondly, to assess whether the association between cortisol and delirium is stress-related or mediated by other pathologies, such as major depressive disorder (MDD) or cognitive impairment.MethodsThe patients were examined one day preoperatively with Mini International Neuropsychiatric Interview and Montreal Cognitive Assessment to screen for depression and cognitive impairment, respectively. Blood samples for cortisol levels were collected both pre- and post-operatively. The Confusion Assessment Method was used within the first five days postoperatively to screen for a diagnosis of delirium.ResultsPostoperative delirium developed in 36% (41of 113) of participants. Multivariate logistic regression analysis revealed two groups independently associated with an increased risk of developing post-operative delirium:Those with pre-operatively raised cortisol levels andThose with a pre-operative diagnosis of MDD associated with raised levels of cortisol post-operatively. According to ROCanalysis the most optimal cutoff values of the preoperative and postoperative cortisol concentration which predict the development of delirium were 353.55 nmol/L, and 994.10 nmol/L, respectively.ConclusionRaised peri-operative plasma cortisol concentrations are associated with delirium after CABG surgery. This may be an important pathophysiological consideration in the increased risk of post-operative delirium seen in patients with a preoperative diagnosis of MDD.

Emergence delirium: a narrative review

“…Another study, by Lim at al., attempted to explain the neurophysiology behind hyperexcitatory behaviors occurring after sevoflurane anesthesia [23]. They postulated that the excitation may result from the potentiation by sevoflurane of GABAergic depolarization/excitation in neocortical neurons, cells implicated in the genesis of arousal and consciousness.…”

“…Their study employed behavioral tests and electrophysiological recordings in neocortical slice preparations, the results of which found that sevoflurane produced post-anesthetic hyperexcitatory behaviors (PAHBs) in postnatal day 1-15 rats. On the basis of their results, they concluded that sevoflurane may produce PAHBs by potentiating GABAergic depolarization/excitation in neocortical neurons [23].…”