Eligibility for elective surgery in patients recovering from mild COVID-19: A propensity-matched analysis.

OBJECTIVE: To study the timing of surgery after a recent Omicron variant infection, to provide a reference for policymakers, clinicians, and patients. METHODS: This single-center propensity-matched analysis was designed and reported according to the EQUATOR-STROBE guidelines. Patients recovering from COVID-19 infection were divided into three groups based on the period from disappearance of respiratory symptoms to surgery: ≤7 days, 8-14 days, and >14 days groups. Outcome measures included postoperative respiratory complications, vascular thrombosis, myocardial infarction, ischemic stroke, and mortality. RESULTS: Between August 1 and December 31, 2022, 9023 surgical procedures were performed, of which 7490 surgeries met the inclusion criteria. Propensity matching resulted in a final cohort of 227 patients recovered from COVID-19 and 2043 SARS-CoV-2 negative patients. Compared with the SARS-CoV-2 negative group, the incidence of postoperative respiratory complications was significantly higher (15.91% vs. 6.71%, p = 0.028) only in the ≤7 days group. There were no statistically significant differences in the other 30-day outcomes between the SARS-CoV-2 negative and the three COVID-19 recovery groups. CONCLUSIONS: Patients who have recovered from mild COVID-19 may be eligible for elective surgery at least 7 days after recovery, since they do not have an increased risk of postoperative complications or mortality within 30 days.

LXA4 attenuates perioperative neurocognitive disorders by suppressing neuroinflammation and oxidative stress.

Perioperative neurocognitive disorder (PND) is a common complication that increases morbidity and mortality in elderly patients undergoing surgery. Abnormal microglia activation causes neuroinflammation and contributes to the development of PND. Growing evidence shows that lipoxin A4 (LXA4), a lipid mediator, possesses potent anti-inflammatory activities. In this study, we investigated whether LXA4 exerted a protective effect against surgery-induced neurocognitive deficits and explored the underlying mechanisms. Mice were subjected to laparotomy under sevoflurane anesthesia to establish an animal model of PND. LXA4 (15 µg/kg/d, ip) was administered three days prior surgery. We showed that LXA4 significantly alleviated surgery-induced cognitive impairments, attenuated neuroinflammation and microglial activation in hippocampus. In BV2 microglial cells treated with LPS (100 ng/mL), pre-application of LXA4 (100 nΜ) significantly inhibited M1 polarization and promoted M2 polarization, and decreased the levels of pro-inflammatory cytokines (IL-1ß, TNF-α, IL-6) and increased the levels of anti-inflammatory cytokine (IL-10). LXA4 also mitigated LPS-regulated expression of HO-1, NOX2, and SOD1, elevated SOD activity, and attenuated ROS production. Furthermore, we revealed that LXA4 increased the expression of SIRT1 and decreased the protein level of acetylated NF-κB p65. SIRT1 inhibitor EX-527 abolished the anti-inflammatory and antioxidant response effects of LXA4 in BV2 microglial cells. Hence, LXA4 is a potential therapeutic agent for surgery-induced neuroinflammation, oxidative stress, and cognitive deficit, and the effect of LXA4 is probably mediated by the activation of the SIRT1/NF-κB signaling pathway in microglia.