Predictors of Mortality and Effect of Drug Therapies in Mechanically Ventilated Patients With Coronavirus Disease 2019: A Multicenter Cohort Study.

We conducted a multicenter cohort study to determine the effect of drug therapies on survival in mechanically ventilated patients with coronavirus disease 2019. All consecutive adult patients admitted to ICU for coronavirus disease 2019 from March 1, 2020, to April 25, 2020, and under invasive mechanical ventilation for more than 24 hours were included. Out of 2,003 patients hospitalized for coronavirus disease 2019, 361 were admitted to ICU, 257 were ventilated for more than 24 hours, and 247 were included in the study. Simple and multiple time-dependent Cox regression models were used to assess the effects of factors on survival. Methylprednisolone administration during the first week of mechanical ventilation was associated with a decrease in mortality rate from 48% to 34% (p = 0.01). Mortality was significantly associated with older age, higher creatinine, lower lymphocyte count, and mean arterial pressure lower than 70 mm Hg on the day of admission.

Bispectral index profile during carotid cross clamping.

This study aimed at investigating the Bispectral Index (BIS) profile during carotid cross clamping (CXC). The study involved a pilot group of 10 patients undergoing routine carotid endarterectomy with shunt insertion under total intravenous anesthesia, and a study group of 26 additional patients. In all patients, rates of propofol and remifentanil providing a steady-state level of hypnosis (BIS: 40-60) were maintained constant throughout a recording period ranging from 3 minutes before CXC to shunt insertion. BIS was recorded throughout this period and the internal carotid backflow observed at the time of shunt insertion was graded as good, moderate, or poor. In addition, A-Line Autoregressive Index (AAI) and processed electroencephalogram (EEG) parameters were recorded in patients of the study group. All parameters were averaged over 1 minute before CXC, at CXC, 1, 2, and 3 minutes after CXC, and at shunt insertion. Statistical analysis was performed using chi2, Friedman, and Spearman correlation tests. For technical reasons, reliable AAI, BIS monitor-derived, and other processed EEG data were obtained in 24, 25, and 18 patients of the study group, respectively. During the first 3 minutes after CXC, BIS increased over 60 [68.8 (6.1)] in 47%, decreased below 40 [34.9 (4.4)] in 25%, and remained in the 40 to 60 range in 28% of all recruited patients. A BIS increase was more frequently observed in patients with moderate or poor than in those with good internal carotid backflow (78, 67, and 29%, respectively). It was significantly correlated to an increase in AAI and EEG amplitude, a decrease in EEG suppression ratio, and a shorter time between induction of anesthesia and CXC. A BIS decrease was significantly correlated to an increase in suppression ratio and a longer time between induction and CXC. In conclusion, during CXC under a constant level of intravenous anesthesia, BIS may increase, decrease, or remain unchanged. The paradoxical BIS increase could be related to borderline ischemia, a change in brain anesthetic agent concentration, or a change in the nociceptive-antinociceptive balance associated with a CXC-elicited painful stimulation. Caution should be used when interpreting BIS value during CXC.

Biomarkers of oxidative stress in critically ill patients: what should be measured, when and how?

PURPOSE OF REVIEW: This review is dedicated to updating the knowledge on oxidative stress in critically ill patients with an intense inflammatory reaction, and to link it with recent findings supporting the possible involvement of oxidative injuries in systems and organs that frequently fail in the critically ill. RECENT FINDINGS: Some direct or indirect biomarkers of oxidative stress have been validated in critically ill patients, and further support the major role of oxidative stress in these conditions. SUMMARY: The assessment of oxidative stress, defined as the association between an increased production of oxygen-derived species and an exhaustion of the stores of antioxidants, requires a multimodal approach. Oxidative damage itself can be much better estimated by quantifying the oxidative byproducts of the lipids and proteins associated with an evaluation of the remaining stores of the corresponding functional antioxidants, or the activity of antioxidant enzymes, than by global tests of the total oxidative damage or the total antioxidant stores. Recent clinical data confirm an important role of increased oxidative stress in the acute dysfunctions of the respiratory, renal and cerebral systems.