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Background and objectives: Anesthesiologists and hospitals are increasingly confronted with costs associated with the complications of Peripheral Nerve Blocks (PNB) procedures. The objective of our study was to identify the incidence of the main adverse events associated with regional anesthesia, particularly during anesthetic PNB, and to evaluate the associated healthcare and social costs. Methods: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we conducted a systematic search on EMBASE and PubMed with the following search strategy: (“regional anesthesia” OR “nerve block”) AND (“complications” OR “nerve lesion” OR “nerve damage” OR “nerve injury”). Studies on patients undergoing a regional anesthesia procedure other than spinal or epidural were included. Targeted data of the selected studies were extracted and further analyzed. Results: Literature search revealed 487 articles, 21 of which met the criteria to be included in our analysis. Ten of them were included in the qualitative and 11 articles in the quantitative synthesis. The analysis of costs included data from four studies and 2,034 claims over 51,242 cases. The median claim consisted in 39,524 dollars in the United States and 22,750 pounds in the United Kingdom. The analysis of incidence included data from seven studies involving 424,169 patients with an overall estimated incidence of 137/10,000. Conclusions: Despite limitations, we proposed a simple model of cost calculation. We found that, despite the relatively low incidence of adverse events following PNB, their associated costs were relevant and should be carefully considered by healthcare managers and decision makers.

ABSTRACT: Objectives: Severe trauma patients are at higher risk of infection and often exposed to antibiotics, which could favor acquisition of antimicrobial resistance. In this study, we aimed to assess prevalence, acquisition, and factors associated with acquisition of extended-spectrum cephalosporin-resistant Gram-negative bacteria (ESCR-GNB) in severe trauma patients. Methods: We conducted a retrospective monocentric cohort study in a French level one Regional Trauma Centre between 01 January 2010and 31 December 2015. Patients admitted for ≥ 7 days, with an Injury Severity Score ≥ 15, and ≥ 1 microbiological sample were included in the analysis. Prevalence and acquisition rate of ESCR-GNB were determined then, factors associated with ESCR-GNB acquisition were assessed using a Cox model. Results: Of 1873 patients admitted during the study period, 507 were included (median Injury Severity Score = 29 [22–34] and median intensive care unit length of stay = 16 days [10–28]). Most of them (450; 89%) had an antimicrobial therapy. Prevalence of ESCR-GNB increased from 13% to 33% during intensive care unit stay, bringing the ESCR-GNB acquisition rate to 29%. Acquisition of ESCR-GNB was mainly related to AmpC beta-lactamase Enterobacterales and was independently associated with mechanical ventilation needs (hazard ratio [HR] = 6.39; 95% confidence interval [CI] [1.51–27.17]; P = 0.01), renal replacement therapy needs (HR = 2.44; 95% CI [1.24–4.79]; P = 0.01), exposure to cephalosporins (HR = 1.06; 95% CI [1.01–1.12]; P = 0.02), and/or combination therapy with non-beta-lactam antibiotics such as vancomycin, linezolid, clindamycin, or metronidazole (HR = 1.03; 95% CI [1.01–1.06]; P = 0.02). Conclusions: Acquisition of ESCR-GNB was prevalent in severe trauma patients. Our results suggest selecting antibiotics with caution, particularly in the most severely ill.

Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare type of leukodystrophy, in the majority of cases caused by mutations in the MLC1 gene. MRI from MLC patients shows diffuse cerebral white matter signal abnormality and swelling, with evidence of increased water content. Histopathology in a MLC patient shows vacuolation of myelin, which causes the cerebral white matter swelling. MLC1 protein is expressed in astrocytic processes that are part of blood- and cerebrospinal fluid-brain barriers. We aimed to create an astrocyte cell model of MLC disease. The characterization of rat astrocyte cultures revealed MLC1 localization in cell–cell contacts, which contains other proteins described typically in tight and adherent junctions. MLC1 localization in these contacts was demonstrated to depend on the actin cytoskeleton; it was not altered when disrupting the microtubule or the GFAP networks. In human tissues, MLC1 and the protein Zonula Occludens 1 (ZO-1), which is linked to the actin cytoskeleton, co-localized by EM immunostaining and were specifically co-immunoprecipitated. To create an MLC cell model, knockdown of MLC1 in primary astrocytes was performed. Reduction of MLC1 expression resulted in the appearance of intracellular vacuoles. This vacuolation was reversed by the co-expression of human MLC1. Re-examination of a human brain biopsy from an MLC patient revealed that vacuoles were also consistently present in astrocytic processes. Thus, vacuolation of astrocytes is also a hallmark of MLC disease.