高质量的心肺复苏是救治心脏停搏的主要手段,复苏后的优化治疗和护理为患者的生存提供了保障,但疾病的高致死率、致残率仍然是目前的主要问题.各种床旁监测技术在心肺复苏中的应用日渐成熟,它们能否为急诊心肺复苏提供评估、预测价值,并取得好的临床结局,也是进一步研究的方向.通过对床旁即时超声、近红外光谱、即时检验、脑电图监测等技术的研究进行综述,阐述了各项技术应用的主要适应症及存在的问题,认为床旁监测技术的应用实现了多模式监测,为心肺复苏中的指导和预测提供了可能.

Objective: To investigate the application effect of extracorporeal membrane oxygenation (ECMO) in patients with severe acute respiratory distress syndrome (ARDS) caused by Pneumocystis jirovecii pneumonia (PJP) after kidney transplantation. Methods: This is a case series on 10 kidney transplant recipients with severe ARDS caused by PJP at the People’s Hospital of Zhengzhou, who were enrolled as the case group. A total of 17 cases of PJP diagnosed with severe ARDS without ECMO were selected as the control group. The timing and mode of ECMO support and treatment complications were summarized. The primary aim of this study was mortality and secondary was imaging and complications. Results: The enrolled patients’ oxygenation index before the start of ECMO ranged from 25 to 92, and the time from admission to the start of ECMO was 1–17 days, with an average of 5.56 days. In the case group, one patient died of hemorrhagic shock due to abdominal hemorrhage, but the other nine patients were successfully weaned from ECMO. Of these patients, one died due to sepsis following weaning. The survival rate in the case group was 80.0% (8/10), and the survival rate in the control group was 35.29% (6/17). The vein–vein ECMO support time in the nine successfully weaned patients in the case group ranged from 131 to 288 h, with an average of 215.5 h. Of the eight patients who survived, deterioration of renal function after transplantation occurred in two patients, but no fatal complications occurred. Conclusion: Overall, Patients with severe ARDS caused by postoperative PJP infection following kidney transplantation have a poor prognosis. The mortality was lower in patients who were treated with ECMO compared to standard care.

Sepsis-associated encephalopathy (SAE) is a common and severe complication of sepsis. The cognitive dysfunction that ensues during SAE has been reported to be caused by impairments of the hippocampus. Microglia serves a key role in neuroinflammation during SAE through migration. Forkhead box C1 (Foxc1) is a member of the forkhead transcription factor family that has been found to regulate in cell migration. However, the role of Foxc1 in neuroinflammation during SAE remains unknown. In the present study, the mechanistic role of Foxcl on microglial migration, neuroinflammation and neuronal apoptosis during the occurrence of cognitive dysfunction in SAE was investigated. A microglia-mediated inflammation model was induced by LPS in BV-2 microglial cells in vitro, whilst a SAE-related cognitive impairment model was established in mice using cecal ligation and perforation (CLP) surgery. Cognitive function in mice was evaluated using the Morris Water Maze (MWM) trial. Lipopolysaccharide (LPS) treatment was found to trigger BV-2 cell migration, inflammation and neuronal apoptosis. In addition, CLP surgery induced cognitive injury, which was indicated by longer latencies and shorter dwell times in the goal quadrant compared with those in the Sham group in the MWM trial. LPS treatment or CLP induction decreased the expression of Foxc1 and inhibitor of NF-kappa B (I kappa B alpha) whilst increasing that of p65, IL-1 beta and TNF-alpha. After Foxc1 was overexpressed, the cognitive dysfunction of mice that underwent CLP surgery was improved, with the expression of I kappa B alpha also increased, microglial cell migration, the expression of p65, IL-1 beta and TNF-alpha and neuronal apoptosis were all decreased in vivo and in vitro, which were in turn reversed by the inhibition of I kappa B alpha in vitro. Overall, these results suggest that the overexpression of Foxc1 inhibited microglial migration whilst suppressing the inflammatory response and neuronal apoptosis by regulating the I kappa B alpha/NF-kappa B pathway, thereby improving cognitive dysfunction during SAE.