Effect of chlorhexidine skin prep and subcuticular skin closure on post-operative infectious morbidity and wound complications following cesarean section

Abstract: Background: The obstetrical department at University of Iowa implemented several interventions at reducing post-operative infections and wound complication rates following a cesarean delivery. We implemented subcuticular closure of the skin following all cesarean sections in February of 2011 and switched from a povidone/iodine skin prep to a chlorhexidine-alcohol prep April 19th 2011. Based on prior studies, we hypothesized a 50% reduction in post cesarean wound complications Objective: To determine if changes in skin prep type and closure method decreases post-operative infectious morbidity and wound complications. Methods: The study reviewed charts of women who underwent a cesarean section between 7/1/2010 and 12/31/2010 compared to those that underwent a cesarean section between 4/19/2011 and 9/7/2011. A total of 568 charts were reviewed. Women were divided into two groups; the control group included those who had a povidone/iodine skin prep and staple closure, the intervention group included those women who had chlorhexidine skin prep and skin closure with subcuticular suture. Results: A total of 568 charts were reviewed and 190 control (iodine/staples) subjects and 139 intervention (chlorhexidine-alcohol/suture) subjects were identified. We found no statistical difference in the overall wound complication rates between the control and intervention groups, 22.1% vs 17.4% (p.22). We did however find a significant decrease in wound separation rates: 8.4% vs 3% (p.014) Analysis showed significant risk factors for infectious morbidity and wound separation to be labor prior to surgery (p Conclusion: In our population the implementation of a chlorhexidine skin prep and closure of the skin with a subcuticular suture did not decrease overall infectious morbidity, it did however decrease our wound separation rate

Cervical keratinocytes containing stably replicating extrachromosomal HPV-16 are refractory to transformation by oncogenic H-Ras

AbstractRas expression in human epithelial cells with integrated HPV genomes has been shown to cause tumorigenic transformation. The effects of Ras in cells representing early stage HPV-associated disease (i.e., when HPV is extrachromosomal and the oncogenes are under control of native promoters) have not been examined. Here, we used human cervical keratinocyte cell lines containing stably replicating extrachromosomal HPV-16 and present the novel finding that these cells resist transformation by oncogenic H-Ras. Ras expression consistently diminished anchorage-independent growth (AI), reduced E6 and E7 expression, and caused p53 induction in these cells. Conversely, AI was enhanced or maintained in Ras-transduced cervical cells that were immortalized with a 16E6/E7 retrovirus, and minimal effects on E6 and E7 expression were observed. Ras expression with either episomal HPV-16 or LXSN-E6/E7 was insufficient for tumorigenic growth suggesting that other events are needed for tumorigenic transformation. In conclusion, our results indicate that Ras-mediated transformation depends on the context of HPV oncogene expression and that this is an important point to address when developing HPV tumor models