Surgical decompression combined with antimicrobial therapy remains the recommended treatment. In addition to abscess locations and motor deficits, inflammatory markers such as WBC counts and C-reactive protein levels are prognostic for outcomes.

BackgroundPostoperative delirium (POD) occurs frequently after cardiac surgery and is associated with increased morbidity and mortality. We analysed whether perioperative bilateral BIS monitoring may detect abnormalities before the onset of POD in cardiac surgery patients.MethodsIn a prospective observational study, 81 patients undergoing cardiac surgery were included. Bilateral Bispectral Index (BIS)-monitoring was applied during the pre-, intra- and postoperative period, and BIS, EEG Asymmetry (ASYM), and Burst Suppression Ratio (BSR) were recorded. POD was diagnosed according to the Confusion Assessment Method for the Intensive Care Unit, and patients were divided into a delirium and non-delirium group.ResultsPOD was detected in 26 patients (32%). A trend towards a lower ASYM was observed in the delirium group as compared to the non-delirium group on the preoperative day (ASYM = 48.2 ± 3.6% versus 50.0 ± 4.7%, mean ± sd, p = 0.087) as well as before induction of anaesthesia, with oral midazolam anxiolysis (median ASYM = 49.5%, IQR [47.4;51.5] versus 50.6%, IQR [49.1;54.2], p = 0.081). Delirious patients remained significantly (p = 0.018) longer in a burst suppression state intraoperatively (107 minutes, IQR [47;170] versus 44 minutes, IQR [11;120]) than non-delirious patients. Receiver operating analysis revealed burst suppression duration (area under the curve = 0.73, p = 0.001) and BSR (AUC = 0.68, p = 0.009) as predictors of POD.ConclusionsIntraoperative assessment of BSR may identify patients at risk of POD and should be investigated in further studies. So far it remains unknown whether there is a causal relationship or rather an association between intraoperative burst suppression and the development of POD.Trial registrationclinicaltrials.gov NCT01048775

Background and Purpose-Disturbances of cerebrovascular autoregulation are thought to be involved in delayed cerebral ischemia and infarction after aneurysmal subarachnoid hemorrhage (SAH). We hypothesized that the continuous monitoring of brain tissue oxygen (PtiO 2 ) pressure reactivity enables the detection of impaired autoregulation after SAH and that impaired autoregulation is associated with delayed infarction. Methods-In 67 patients after severe SAH, continuous monitoring of cerebral perfusion pressure (CPP) and PtiO 2 was performed for an average of 7.4 days. For assessment of autoregulation, the index of PtiO 2 pressure reactivity (ORx) was calculated as a moving correlation coefficient between values of CPP and PtiO 2 . Higher ORx values indicate disturbed autoregulation, whereas lower ORx values signify intact autoregulation. Results-Twenty patients developed delayed cerebral infarction, and 47 did not. Mean ORx was significantly higher in the infarction group compared with the noninfarction group (0.43Ϯ0.09 vs 0.23Ϯ0.14, respectively; PϽ0.0001). In a day-by-day analysis, ORx did not differ between groups from days 1 to 4 after SAH but was significantly higher from day 5 onward in the infarction group, indicating a deficit of autoregulatory capacity. In a logistic-regression model, ORx values from days 5 and 6 after SAH carried predictive value for the occurrence of delayed infarction but before this event ultimately occurred (Pϭ0.003). Conclusions-ORx

The moving correlation coefficients between slow changes of arterial blood pressure and mean or systolic flow velocity, termed "Mx" and "Sx," respectively, characterize cerebral autoregulation but have not been applied to subarachnoid hemorrhage. A study in 15 patients revealed that Mx and Sx were significantly increased, indicating impaired autoregulation during vasospasm as compared with baseline, as well as on the side of vasospasm in comparison with the contralateral side.

ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.