Background: Anesthesia given to immature rodents causes cognitive decline, raising the possibility that the same might be true for millions of children undergoing surgical procedures under general anesthesia each year. We tested the hypothesis that anesthesia-induced cognitive decline in rats is treatable. We also tested if anesthesia-induced cognitive decline is aggravated by tissue injury. Methods: Seven-day old rats underwent sevoflurane anesthesia (1 minimum alveolar concentration, 4 h) with or without tail clamping. At 4 weeks, rats were randomized to environmental enrichment or normal housing. At 8 weeks rats underwent neurocognitive testing, which consisted of fear conditioning, spatial reference memory, and water maze-based memory consolidation tests, and interrogated working memory, short-term memory, and early long-term memory. Results: Sevoflurane-treated rats had a greater escape latency when the delay between memory acquisition and memory retrieval was increased from 1 min to 1 h, indicating that short-term memory was impaired. Delayed environmental enrichment reversed the effects of sevoflurane on short-term memory and generally improved many tested aspects of cognitive function, both in sevoflurane-treated and control animals. The performance of tail-clamped rats did not differ from those rats receiving anesthesia alone. Conclusion: Sevoflurane-induced cognitive decline in rats is treatable. Delayed environmental enrichment rescued the sevoflurane-induced impairment in short-term memory. Tissue injury did not worsen the anesthesia-induced memory impairment. These findings may have relevance to neonatal and pediatric anesthesia.

Prolonged postoperative decrease in lung function is common after major upper abdominal surgery. Evidence suggests that ventilation with low tidal volumes may limit the damage during mechanical ventilation. We compared postoperative lung function of patients undergoing upper abdominal surgery, mechanically ventilated with high or low tidal volumes. This was a double-blind, prospective, randomized controlled clinical trial. One hundred and one patients (age ≥50 yr, ASA ≥II, duration of surgery ≥3 h) were ventilated with: (i) high [12 ml kg⁻¹ predicted body weight (PBW)] or (ii) low (6 ml kg⁻¹ PBW) tidal volumes intraoperatively. The positive end-expiratory pressure was 5 cm H₂O in both groups and breathing frequency adjusted to normocapnia. Time-weighted averages (TWAs) of forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV₁) until 120 h after operation were compared (P<0.025 considered statistically significant). Secondary outcomes were oxygenation, respiratory and non-respiratory complications, length of stay and mortality. The mean (sd) values of TWAs of FVC and FEV₁ were similar in both groups: FVC: 6 ml group 1.8 (0.7) litre vs 12 ml group 1.6 (0.5) litre (P=0.12); FEV₁: 6 ml group 1.4 (0.5) litre vs 12 ml group 1.2 (0.4) litre (P=0.15). FVC and FEV₁ at any single time point and secondary outcomes did not differ significantly between groups. Prolonged impaired lung function after major abdominal surgery is not ameliorated by low tidal volume ventilation.

Background: Mechanical power during ventilation estimates the energy delivered to the respiratory system through integrating inspiratory pressures, tidal volume, and respiratory rate into a single value. It has been linked to lung injury and mortality in the acute respiratory distress syndrome, but little evidence exists regarding whether the concept relates to lung injury in patients with healthy lungs. This study hypothesized that higher mechanical power is associated with greater postoperative respiratory failure requiring reintubation in patients undergoing general anesthesia. Methods: In this multicenter, retrospective study, 230,767 elective, noncardiac adult surgical out- and inpatients undergoing general anesthesia between 2008 and 2018 at two academic hospital networks in Boston, Massachusetts, were included. The risk-adjusted association between the median intraoperative mechanical power, calculated from median values of tidal volume (V_t), respiratory rate (RR), positive end-expiratory pressure (PEEP), plateau pressure (P_plat), and peak inspiratory pressure (P_peak), using the following formula: mechanical power (J/min) = 0.098 × RR × V_t × (PEEP + ½[P_plat – PEEP] + [P_peak − P_plat]), and postoperative respiratory failure requiring reintubation within 7 days, was assessed. Results: The median intraoperative mechanical power was 6.63 (interquartile range, 4.62 to 9.11) J/min. Postoperative respiratory failure occurred in 2,024 (0.9%) patients. The median (interquartile range) intraoperative mechanical power was higher in patients with postoperative respiratory failure than in patients without (7.67 [5.64 to 10.11] vs. 6.62 [4.62 to 9.10] J/min; P < 0.001). In adjusted analyses, a higher mechanical power was associated with greater odds of postoperative respiratory failure (adjusted odds ratio, 1.31 per 5 J/min increase; 95% CI, 1.21 to 1.42; P < 0.001). The association between mechanical power and postoperative respiratory failure was robust to additional adjustment for known drivers of ventilator-induced lung injury, including tidal volume, driving pressure, and respiratory rate, and driven by the dynamic elastic component (adjusted odds ratio, 1.35 per 5 J/min; 95% CI, 1.05 to 1.73; P = 0.02). Conclusions: Higher mechanical power during ventilation is statistically associated with a greater risk of postoperative respiratory failure requiring reintubation. Editor’s Perspective: What We Already Know about This Topic: What This Article Tells Us That Is New: