Brain mineralization in postoperative delirium and cognitive decline
Lammers-Lietz, F.; Borchers, F.; Feinkohl, I.; Hetzer, S.; Kanar, C.; Lachmann, G.; Chien, C.; Spies, C.; Winterer, G.; Zaborszky, L.; Zacharias, N.; Paul, F.
Show abstract
Delirium is a severe postoperative complication associated with poor overall and especially neurocognitive prognosis. Altered brain mineralization is found in neurodegenerative disorders but has not been studied in postoperative delirium and postoperative cognitive decline. We hypothesized that mineralization-related hypointensity in susceptibility-weighted magnetic resonance imaging (SWI) is associated with postoperative delirium and cognitive decline. We analyzed a subsample of cognitively healthy patients [≥]65 years presenting for elective major surgery who underwent SWI before (N=65) and three months after surgery (N=33) as part of a subproject in the BioCog study. We measured relative SWI intensities in basal ganglia, hippocampus, and posterior basal forebrain cholinergic system (pBFCS). A post-hoc analysis of two pBFCS subregions (Ch4, Ch4p) was conducted. Patients were screened for delirium until the seventh postoperative day. Cognitive testing was performed before and three months after surgery. Preoperative relative SWI hypointensities in the basal ganglia and pBFCS were associated with increased risk for postoperative delirium after adjustment for surgery duration. After additional adjustment for age, sex, preoperative MMSE and region volume, only the association of pBFCS hypointensity and postoperative delirium remained significant. Adjusted for surgery duration, perioperative change in relative SWI intensities of the pBFCS was associated with cognitive decline three months after surgery. This association remained at a trend level after adjustments for age, sex, and region volume, but a significant independent association especially with pBFCS-subregion Ch4p was found in a post-hoc analysis. Brain mineralization, particularly in the cerebral cholinergic system, could be a pathomechanism in postoperative delirium and cognitive decline.
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