Association of an Obstetric Surgical Closing Protocol With Infection After Cesarean Delivery.

OBJECTIVE: To examine surgical site infection rates before and after the addition of a closing protocol to an existing surgical site infection risk-reduction bundle used during cesarean delivery. METHODS: We conducted a single-center retrospective cohort study to review the association of a closing protocol with rates of surgical site infection after cesarean delivery. The closing protocol included fresh surgical instruments and physician and scrub nurse glove change before fascia closure. Surgical site infections were defined using Centers for Disease Control and Prevention criteria. Eligible patients underwent cesarean delivery at our institution from July 1, 2013, through December 31, 2015 (n=1,708; preimplementation group), or from June 1, 2016, through April 30, 2018 (n=1,228; postimplementation group). RESULTS: The surgical site infection rate was 2.3% preimplementation and 2.7% postimplementation (difference 0.4%, 95% CI -1.6 to 0.7%]. The mean [SD] duration of the surgical procedure was longer postimplementation (59.6 [23.7] vs 55.6 [21.5] minutes; P<.001). CONCLUSION: Addition of a closing tray and glove change to our existing surgical site infection risk-reduction bundle was not associated with a reduction in the frequency of postcesarean surgical site infection but was associated with longer operating times.

Increased cell-free fetal DNA release after apoptosis and sterile inflammation in human trophoblast cells.

PROBLEM: Cell-free fetal DNA (cffDNA) shed from the placenta can be detected in maternal blood and increases incrementally during gestation. Concentrations are further elevated with pregnancy complications. Specific activators of cffDNA release in such complications have not been identified. Here, we use trophoblast cells from early and term placenta to examine cffDNA release following apoptosis, infection, and sterile inflammatory stress. METHOD OF STUDY: HTR8/SVneo cells were used to model first-trimester trophoblasts, and term cytotrophoblasts (CTBs) were isolated from placentae collected after uncomplicated deliveries. Trophoblasts were treated with varying concentrations of doxorubicin (DOX), lipopolysaccharide (LPS), or high-mobility group box protein 1 (HMGB1) for 18 h. Cells or supernatants were quantified for caspase-3/7 cleavage, pro-inflammatory cytokine secretion, and cffDNA release. RESULTS: Both HTR8/SVneo and CTBs underwent caspase-3/7 cleavage following DOX treatment, with HTR8/SVneo cells more sensitive to apoptosis than term CTBs. Apoptotic cells released more cffDNA in a dose-dependent manner. Treatment with LPS resulted in an increase in pro-inflammatory IL-6 release, particularly in term CTBs compared to early trophoblasts; however, LPS did not affect cffDNA release. Lastly, while neither cell released more TNF-α following stimulation with HMGB1, both HTR8/SVneo and CTBs released significantly more cffDNA in the presence of HMGB1. CONCLUSIONS: These data show that apoptosis and sterile inflammation induced by DOX and HMGB1, respectively, cause an increase in cffDNA concentrations in both first-trimester and term trophoblasts. Understanding physiologic release of cffDNA during healthy and complicated pregnancy can identify new targets for the diagnosis and treatment of gestational complications.