Xenon anaesthesia produces better early postoperative cognitive recovery than sevoflurane anaesthesia.

BACKGROUND AND OBJECTIVE: Xenon anaesthesia may have the potential to reduce postoperative cognitive impairment after general anaesthesia. This randomized double-blind controlled trial was designed to compare the early postoperative cognitive recovery after xenon and sevoflurane anaesthesia. METHODS: After institutional ethics approval, we obtained informed written consent from 60 adults, with American Society of Anesthesiologists I or II status, scheduled for elective surgery with an estimated surgery time between 60 and 360 min. Patients were randomized to receive xenon or sevoflurane anaesthesia. Both groups received a remifentanil infusion adjusted to clinical needs based on patients' haemodynamic and state entropy of less than 60. In cases of state entropy of at least 60 during the first 15 min after induction, patients in the xenon group received a propofol infusion targeted to state entropy of less than 60. The primary end-point of the study was the early postoperative cognitive recovery evaluated by the Short Orientation Memory Concentration Test. RESULTS: There was no significant difference in the mean preoperative Short Orientation Memory Concentration Test values between groups (sevoflurane 2.7 +/- 3.2 and xenon 3.2 +/- 2.6; P, 0.53). Awakening was significantly faster in the xenon group (sevoflurane 8 +/- 4 min and xenon 3 +/- 1 min; P < 0.001). Patients receiving xenon presented significantly lower Short Orientation Memory Concentration Test scores at 30 min (sevoflurane 6.7 +/- 5.9 and xenon 3.3 +/- 3.1; P 0.003) and 60 min (xenon 2.1 +/- 3 and sevoflurane 5 +/- 4.1; P 0.003) after extubation. CONCLUSION: Xenon anaesthesia was associated with faster emergence and with better early postoperative cognitive recovery than sevoflurane anaesthesia.

Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: an experimental study.

OBJECTIVE: We report the evolution of severe ventilator-induced lung injury associated with lethal systemic capillary leak syndrome, when sheep were ventilated at a peak inspiratory pressure of 50 cm H2O, at a respiratory rate of 8 breaths.min, with an inspiratory time of 2.5 secs. DESIGN: A prospective laboratory animal study. SETTING: Experimental animal research laboratory. SUBJECTS: Mixed breed sheep. INTERVENTIONS: Sheep were anesthetized, paralyzed, and mechanically ventilated. MEASUREMENTS AND MAIN RESULTS: This sheep model was characterized by a rapidly evolving massive anasarca, hemoconcentration, cardiac dysfunction, multiple system organ failure, and severe ventilator-induced lung injury. Cardiovascular changes and profound hemoconcentration developed within 6 hrs from the start of mechanical ventilation, along with a major decline in pulmonary compliance and deterioration in arterial blood gases. When total static lung compliance decreased to 0.15 mL (cm H2O)(-1) x kg(-1) (7-30 hrs), the sheep were randomized to two groups. Group I received high (recruitive) positive end-expiratory pressure (9-20 cm H2O), adjusted as needed; group II received low (supportive) positive end-expiratory pressure (2-6 cm H2O). Sheep in both groups progressively deteriorated and died with cardiocirculatory failure and multiple system organ failure within 12-24 hrs from start of treatment. CONCLUSIONS: This model of lethal systemic capillary leak syndrome with multiple system organ failure differs greatly from our previous sheep model of acute ventilator-induced lung injury in which sheep were ventilated with a peak inspiratory pressure of 50 cm H2O, a respiratory rate of 4 breaths x min(-1), and an inspiratory time of 1.35 secs, without inducing capillary leak syndrome. The mere change of respiratory rate from 4 to 8 breaths x min(-1), with a near doubling of the inspiratory time to 2.5 secs, although maintaining eucapnia, resulted in lethal systemic capillary leak syndrome and multiple system organ failure with both gross and microscopic pathology of lungs greatly different from our previous model of mechanical ventilation-induced acute respiratory distress syndrome.