Objectives: Postoperative delirium (POD) is the most common complication in patients after hip fracture surgery, and the incidence of POD is associated with mortality and disability in patients following hip fracture surgery. Therefore, this study aimed to identify the individual as well as anesthetic and operative risk factors associated with the POD in adult patients after hip fracture surgery. Methods: We searched relevant articles published to February 2020 in Cochrane Library, PubMed, and Embase. Studies involving adult patients who underwent hip fracture surgery were regarded as relevant if the studies contained the individual or anesthetic and surgical characteristics of participants. The pooled relative risk ratios (RRs) or weight mean difference of the variables were estimated by the Mantel-Haenszel or Inverse-Variance methods. Results: A total of 44 studies were included, which altogether included 104572 participants with hip fracture surgery (17703 patients with POD and 86869 patients without POD) and the incidence of POD was 16.93%. A total of 14 risk factors, classified into two categories which were individual as well as anesthetic and operative factors, were identified originally, which included age (weight mean difference

Introduction: Electrical vagal nerve stimulation is known to decrease gut permeability and alleviate gut injury caused by traumatic hemorrhagic shock. However, the specific mechanism of action remains unclear. Glycocalyx, located on the surface of the intestinal epithelium, is associated with the buildup of the intestinal barrier. Therefore, the goal of our study was to explore whether vagal nerve stimulation affects enterocyte glycocalyx, gut permeability, gut injury, and remote lung injury. Materials and methods: Male Sprague Dawley rats were anesthetized and their cervical nerves were exposed. The rats underwent traumatic hemorrhagic shock (with maintenance of mean arterial pressure of 30–35 mmHg for 60 min) with fluid resuscitation. Vagal nerve stimulation was added to two cohorts of animals before fluid resuscitation, and one of them was injected with methyllycaconitine to block the cholinergic anti-inflammatory pathway. Intestinal epithelial glycocalyx was detected using immunofluorescence. Intestinal permeability, the degree of gut and lung injury, and inflammation factors were also assessed. Results: Vagal nerve stimulation alleviated the damage to the intestinal epithelial glycocalyx and decreased intestinal permeability by 43% compared with the shock/resuscitation phase ( P < 0.05). Methyllycaconitine partly eliminated the effects of vagal nerve stimulation on the intestinal epithelial glycocalyx ( P < 0.05). Vagal nerve stimulation protected against traumatic hemorrhagic shock/fluid resuscitation-induced gut and lung injury, and some inflammatory factor levels in the gut and lung tissue were downregulated after vagal nerve stimulation ( P < 0.05). Conclusions: Vagal nerve stimulation could relieve traumatic hemorrhagic shock/fluid resuscitation-induced intestinal epithelial glycocalyx damage via the cholinergic anti-inflammatory pathway.

BackgroundAcute lung injury (ALI) is a common complication after THS/R, and vagus nerve stimulation (VNS) could alleviate lung injury by activating cholinergic anti-inflammatory pathway (CAP) during traumatic hemorrhagic shock/resuscitation (THS/R). The purpose of this study was to explore the effects of VNS on intestinal epithelial glycocalyx and acute lung injury associated with THS/R.MethodsSprague-Dawley rats were subjected to traumatic hemorrhagic shock/ resuscitation to induce ALI. The measurements of intestinal barrier permeability, intestinal epithelial glycocalyx, and the level of inflammation factors and histology of lung and gut tissue were made in each group.ResultsThe level of TNF-α，IL-6 and MPO in lung and gut tissue were significantly decreased in the VNS-treated group. In addition, the shedding of intestinal epithelial glycocalyx and increased gut barrier permeability were alleviated in the VNS-treated group, and the gut tissue and lung tissue injury were mitigated in the VNS-treated group. However, pretreated with methyllycaconitine could reverse the protective effect of VNS.ConclusionsVNS could relieve lung injury associated with THS/R by alleviating the damage of intestinal epithelial glycocalyx, which might be achieved by activating CAP.