Use of an intraoperative sodium oxychlorosene-based infection prevention protocol to safely decrease postoperative wound infections after spine surgery.

OBJECTIVE: Postoperative infection remains prevalent after spinal surgical procedures. Institutional protocols for infection prevention have improved rates of infection after spine surgery. However, prior studies have focused on only elective surgical patients. The aim of this study was to determine the efficacy of a multiinstitutional intraoperative sodium oxychlorosene-based infection prevention protocol for decreasing rate of infection after instrumented spinal surgery. METHODS: A retrospective analysis was performed at two tertiary care institutions with level I trauma programs, and patients who underwent posterior instrumented spinal fusion between January 1, 2011, and May 31, 2019, were included. Postoperative deep wound infection rates were captured before and after implementation of a multiinstitutional infection prevention protocol. Possible adverse outcomes related to infection prevention techniques were also examined. In addition, consecutive patients treated from January 1, 2018, to May 31, 2019, were prospectively included in a database to collect preoperative and postoperative spine-specific quality of life measures and to assess the impact of postoperative infection on quality of life. RESULTS: A total of 5047 patients fit the inclusion criteria. Of these, 1043 patients underwent surgery prior to protocol implementation. The infection rate of this cohort (3.5%) decreased significantly after protocol implementation (1.2%, p < 0.001). Postoperative sterile seroma rates did not differ between the preprotocol and postprotocol groups (0.7% vs 0.7%, p = 0.5). In the 1031 patients who underwent surgery between January 2018 and May 2019, the fusion rate was 89.2%. Quality of life outcomes between patients with infection and those without infection were similar, although statistical power was limited owing to the low rate of infection. Notably, 2 of 10 patients who developed deep wound infection died of infection-related complications. CONCLUSIONS: An intraoperative sodium oxychlorosene-based infection prevention protocol helped to significantly decrease the rate of infection after spine surgery without negatively impacting other postoperative procedure-related metrics. Postoperative wound infection may be associated with higher-than-expected rate of postoperative mortality.

Clinical characteristics, outcomes and prognosticators in adult patients hospitalized with COVID-19.

BACKGROUND: COVID-19 is a novel disease caused by SARS-CoV-2. METHODS: We conducted a retrospective evaluation of patients admitted with COVID-19 to one site in March 2020. Patients were stratified into 3 groups: survivors who did not receive mechanical ventilation (MV), survivors who received MV, and those who received MV and died during hospitalization. RESULTS: There were 140 hospitalizations; 22 deaths (mortality rate 15.7%), 83 (59%) survived and did not receive MV, 35 (25%) received MV and survived; 18 (12.9%) received MV and died. Thee mean age of each group was 57.8, 55.8 and 72.7 years, respectively (P = .0001). Of those who received MV and died, 61% were male (P = .01). More than half the patients (n = 90, 64%) were African American. First measured d-dimer >575.5 ng/mL, procalcitonin > 0.24 ng/mL, lactate dehydrogenase >445.6 units/L, and brain natriuretic peptide (BNP) >104.75 pg/mL had odds ratios of 10.5, 5, 4.5 and 2.9, respectively for MV (P < .05 for all). Peak BNP >167.5 pg/mL had an odds ratio of 6.7 for inpatient mortality when mechanically ventilated (P = .02). CONCLUSIONS: Age and gender may impact outcomes in COVID-19. D-dimer, procalcitonin, lactate dehydrogenase and BNP may serve as early indicators of disease trajectory.

Evaluation of CpxRA as a Therapeutic Target for Uropathogenic Escherichia coli Infections.

CpxRA is an envelope stress response system found in all members of the family Enterobacteriaceae; CpxA has kinase activity for CpxR and phosphatase activity for phospho-CpxR, a transcription factor. CpxR also accepts phosphate groups from acetyl phosphate, a glucose metabolite. Activation of CpxR increases the transcription of genes encoding membrane repair and downregulates virulence determinants. We hypothesized that activation of CpxR could serve as an antimicrobial/antivirulence strategy and discovered compounds that activate CpxR in Escherichia coli by inhibiting CpxA phosphatase activity. As a prelude to testing such compounds in vivo, here we constructed cpxA (in the presence of glucose, CpxR is activated because of a lack of CpxA phosphatase) and cpxR (system absent) deletion mutants of uropathogenic E. coli (UPEC) CFT073. By RNA sequencing, few transcriptional differences were noted between the cpxR mutant and its parent, but in the cpxA mutant, several UPEC virulence determinants were downregulated, including the fim and pap operons, and it exhibited reduced mannose-sensitive hemagglutination of guinea pig red blood cells in vitro In competition experiments with mice, both mutants were less fit than the parent in the urine, bladder, and kidney; these fitness defects were complemented in trans Unexpectedly, in single-strain challenges, only the cpxA mutant was attenuated for virulence in the kidney but not in the bladder or urine. For the cpxA mutant, this may be due to the preferential use of amino acids over glucose as a carbon source in the bladder and urine by UPEC. These studies suggest that CpxA phosphatase inhibitors may have some utility for treating complex urinary tract infections.