The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.
If you have any questions or comments, please contact us.
Fatal cases of acute shock complicating Clostridium sordellii endometritis following medical abortion with mifepristone (also known as RU-486) used with misoprostol were reported. The pathogenesis of this unexpected complication remains enigmatic. Misoprostol is a pharmacomimetic of PGE(2), an endogenous suppressor of innate immunity. Clinical C. sordellii infections were associated with intravaginal misoprostol administration, suggesting that high misoprostol concentrations within the uterus impair immune responses against C. sordellii. We modeled C. sordellii endometritis in rats to test this hypothesis. The intrauterine but not the intragastric delivery of misoprostol significantly worsened mortality from C. sordellii uterine infection, and impaired bacterial clearance in vivo. Misoprostol also reduced TNF-alpha production within the uterus during infection. The intrauterine injection of misoprostol did not enhance mortality from infection by the vaginal commensal bacterium Lactobacillus crispatus. In vitro, misoprostol suppressed macrophage TNF-alpha and chemokine generation following C. sordellii or peptidoglycan challenge, impaired leukocyte phagocytosis of C. sordellii, and inhibited uterine epithelial cell human beta-defensin expression. These immunosuppressive effects of misoprostol, which were not shared by mifepristone, correlated with the activation of the G(s) protein-coupled E prostanoid (EP) receptors EP2 and EP4 (macrophages) or EP4 alone (uterine epithelial cells). Our data provide a novel explanation for postabortion sepsis leading to death and also suggest that PGE(2), in which production is exaggerated within the reproductive tract during pregnancy, might be an important causal determinant in the pathogenesis of more common infections of the gravid uterus.
OBJECTIVE - To determine whether vaginal preparation with povidone iodine before cesarean decreased the incidence of postpartum infectious morbidity.
METHODS - Participants were randomly assigned to vaginal preparation with povidone iodine (n = 247) or no preparation (n = 251). Postpartum infectious morbidity included fever, defined as temperature of 38C or greater after the day of surgery; endometritis, defined as fever with abdominal or uterine tenderness and initiation of intravenous antibiotics; and wound separation, defined as disruption of the abdominal incision that required wound care. We calculated overall rates of postpartum infectious morbidity, relative risks (RR), and 95% confidence intervals (CI) for the effect of vaginal preparation. As designed and reported, the trial had at least 80% power to detect a 10% or greater absolute difference in rates of overall infectious morbidity, fever, and endometritis (two-tailed, alpha = 0.05).
RESULTS - There was no difference between groups in maternal age, parity, race, education, prior cesarean, type of anesthesia, labor before current cesarean, number of vaginal examinations during labor, internal monitoring, prophylactic antibiotic use, gestational age at delivery, or payment status. Excluding 68 women with chorioamnionitis, incidence of postoperative fever was 19.3%, endometritis 7.2%, and wound separation 7.0%. Vaginal preparation with povidone iodine before cesarean had no effect on risk for fever (RR 1.1, 95% CI 0.8, 1.6), endometritis (RR 1.6, 95% CI 0.8, 3.1), or wound separation (RR 0.6, 95% CI 0.3, 1.3).
CONCLUSION - Vaginal preparation with povidone iodine before cesarean had no effect on the incidence of fever, endometritis, or wound infection.
OBJECTIVE - To examine changes in white blood cell (WBC) count after cesarean and estimate risk of postoperative infection.
METHODS - We measured complete blood cell counts at admission and on postoperative day 1 for 458 women who had cesareans. Information from charts was abstracted, and definitions of infectious outcomes and fever were applied by three physicians masked to laboratory results. We examined changes in absolute and relative WBC counts by labor status. Likelihood ratios for postoperative infection were calculated for statistically distinct categories of percentage changes.
RESULTS - We excluded 60 women with chorioamnionitis. Of the remainder, 34 (8.5%) developed endometritis and three (0.8%) pneumonia. Women who labored before cesarean (n = 198) had higher antepartum (P <.001) and postoperative day 1 (P <.001) WBC counts than those who did not (n = 200). However, change in WBC count after cesarean relative to antepartum was similar for both groups (P =.41), averaging a 22% increase. We grouped percentage changes into the following three levels: up to 24%, 25-99%, and at least 100%. The lowest level (n = 246) corresponded to a category-specific likelihood ratio for diagnosis of serious postpartum infection of 0. 5 (95% confidence interval [CI] 0.3, 0.8), the midlevel (n = 141) to a category-specific likelihood ratio of 1.7 (95% CI 1.2, 2.3), and the highest level (n = 11) to a category-specific likelihood ratio of 5.8 (95% CI 1.8, 18.7).
CONCLUSION - Labor influenced postcesarean WBC counts but did not obscure changes associated with infection. Information gained from changes in WBC counts can be used to assess risk of infection.