Sepsis remains one of the leading causes of death in intensive care units. The early phase of sepsis is characterized by a massive formation of reactive oxygen and nitrogen species such as superoxide and nitric oxide. However, few comprehensive studies on plasma antioxidants have been reported. Increased oxidative stress was confirmed in sepsis patients (n = 18) at the time of hospitalization by a significant decrease in plasma ascorbic acid and a significant increase in the percentage of oxidized form of coenzyme Q10 in total coenzyme Q10 compared to age-matched healthy controls (n = 62). Tissue oxidative damage in patients was suggested by a significant decrease in polyunsaturated fatty acid contents and a significant increase in oleic acid contents in total free fatty acids. Thus, it is reasonable that plasma uric acid (end product of purines) would be significantly elevated. However, uric acid levels were continuously decreased during hospitalization for 7 days, indicating a continuous formation of peroxynitrite. A greater decrease in free cholesterol (FC) compared to cholesterol esters (CE) was observed. Thus, the FC/CE ratio significantly increased, suggesting deficiency of lecithin-cholesterol acyltransferase secreted from the liver. Plasma levels of prosaposin, a coenzyme Q10 binding protein, significantly decreased as compared to healthy controls. This may be correlated with renal injury in sepsis patients, since the kidney is thought to be a major secretor of prosaposin.

In several studies, regional cerebral oxygen saturation (rSO 2 ) has been measured in patients with postcardiac arrest syndrome (PCAS) to analyze the brain's metabolic status. However, the significance of rSO 2 in PCAS patients remains unclear. In the present study, we investigated the relationship between rSO 2 and physiological parameters. Comatose survivors of out-of-hospital PCAS with targeted temperature management (TTM) at 34°C for 24 hours were included. All patients were monitored for their rSO 2 and additional parameters (arterial oxygen saturation [SaO 2 ], hemoglobin [Hb], mean arterial pressure [MAP], arterial carbon dioxide pressure [PaCO 2 ], and body temperature]) measured at the start of monitoring and 24 and 48 hours after return of spontaneous circulation (ROSC). Patients were divided into favorable and unfavorable groups, and the correlation between rSO 2 and these physiological parameters was evaluated by multiple regression analysis. Forty-nine patients were included in the study, with 15 in the favorable group and 34 in the unfavorable group. There was no significant difference in the rSO 2 value between the two groups at any time point. The multiple regression analysis of the favorable group revealed a moderate correlation between rSO 2 and SaO 2 , Hb, and PaCO 2 only at 24 hours (coefficients: 0.482, 0.422, and 0.531, respectively), whereas that of the unfavorable group revealed moderate correlations between rSO 2 and Hb values at all time points, PaCO 2 at 24 hours and MAP at 24 and 48 hours. rSO 2 was moderately correlated to MAP in unfavorable patients. To optimize brain oxygen metabolic balance for PCAS patients with TTM measuring rSO 2 , we suggest total evaluation of each parameters of SaO 2 , Hb, MAP, and PaCO 2 .

Brain injury is the most common cause of death postcardiac arrest. Amplitude-integrated electroencephalography (aEEG) is suggested to be useful in the prognostication in cases of postcardiac arrest brain injury. However, combined monitoring with aEEG and regional oxygen saturation (rSO2) for postcardiac arrest syndrome (PCAS) patients to improve accuracy has not been reported. The purpose of this prospective observational study is to assess the usefulness of aEEG and rSO2 for PCAS patients with targeted temperature management (TTM) to predict neurological outcome and possibly identify the pathophysiology of postcardiac arrest brain injury. PCAS patients with TTM at 34°C were monitored by aEEG and rSO2 immediately after admission to the intensive care unit and evaluated at the start of monitoring, and 24 and 48 hours after return of spontaneous circulation (ROSC). Patients were divided into two groups according to electroencephalography (EEG) pattern: a continuous EEG (C) pattern group and a noncontinuous EEG (NC) pattern group. Patients with C pattern had a significantly more favorable neurologic outcome compared with patients with an NC pattern at each point in time. No significant difference in rSO2 values was observed between the C pattern and the NC pattern at any time point. Variation coefficient at rSO2 in the NC group was significantly greater than that in the C group from the start of the monitoring to 24 hours. aEEG is useful in predicting outcome for PCAS patients whereas rSO2 is not.

It remains uncertain whether neuromonitoring reliably predicts outcome in adult post-cardiac arrest patients in the early stage treated with therapeutic hypothermia. Recent reports demonstrated a regional cerebral oxygen saturation of cardiac arrest patients on hospital arrival could predict their neurological outcome. There has been little discussion about the significance of regional cerebral oxygen saturation in patients with post-cardiac arrest syndrome. Amplitude-integrated electroencephalography monitoring may also provide early prognostic information for post-cardiac arrest syndrome. However, even when the initial electroencephalography is flat after the return of spontaneous circulation, good neurological outcome may still be obtainable if the electroencephalography shifts to a continuous pattern. The electroencephalography varied from flat to various patterns, such as flat, epileptic, or continuous during the first 24 h, while regional cerebral oxygen saturation levels varied even when the electroencephalography was flat. It is therefore difficult to estimate whether regional cerebral oxygen saturation accurately indicates the coupling of cerebral blood flow and metabolism in the early stage after cardiac arrest. Careful assessment of prognosis is necessary when relying solely on regional cerebral oxygen saturation as a single monitoring modality.

Objectives Fatty acids (FAs) have various roles in pro-inflammatory and anti-inflammatory functions. Hypoalbuminemia is often observed in sepsis patients. An imbalance among these compounds formed from FAs caused by hypoalbuminemia may be related to increased mortality in sepsis patients. The purpose of this study was to investigate the correlations between serum albumin and FAs in sepsis and the outcome. Methods This study was an observational investigation. The clinical and laboratory data of sepsis patients were recorded and the Sequential Organ Failure Assessment (SOFA) score was calculated at admission. The serum arachidonic acid (AA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and dihomo-gamma-linolenic acid (DHLA) levels were also measured as FAs. The body mass index (BMI) was used to determine the general nutrition status. Results Two hundred sepsis patients were enrolled during the study period. No significant correlations were observed between the BMI and the SOFA score or the serum albumin level at admission. The FA levels of the non-survivors were significantly lower, but there were no significant differences in the EPA/AA levels of the survivors and non-survivors. A low serum albumin level was closely related to low AA (p<0.0001), EPA (p<0.0001), DHA (p=0.0003), and DHLA levels (p<0.0001). A multiple logistic-regression analysis revealed that a high SOFA score [adjusted odds ratio, 1.19; 95% confidence interval (CI), 1.02-1.39, p=0.026] and low AA (adjusted odds ratio, 0.98; 95% CI, 0.978-0.994, p=0.041) were associated with a poor outcome. Conclusion A lower AA level was an important determinant of the outcome of patients with sepsis. These findings are consistent with the findings of previous studies, which reported that hypoalbuminemia might alter the AA metabolism in sepsis patients.