Sustained reduction in surgical site infection after abdominal hysterectomy.

BACKGROUND: During a period of five years, the rate of surgical site infection (SSI) after abdominal hysterectomy at our institution was >10%. With the implementation of a multifaceted intervention designed to reduce this, the rate of SSI fell to <2% in the post-intervention period. The pre- and post-intervention periods were compared to determine which of the interventions in the multifaceted array of interventions was most valuable in decreasing SSI. METHODS: A retrospective chart review was done to identify: (1) Parameters associated with SSI, and (2) parameters that differed in the pre- and post-intervention periods. The intervention included providing departmental SSI rates to the gynecology faculty, re-educating operating room (OR) staff personnel about appropriate perioperative antibiotic choice and timing, and changing the preferred sterile preparation for abdominal surgery from 10% povidone-iodine (PI) to 4% chlorhexidine gluconate (CHG). The preliminary results of our review also led to the suggestion that surgeons use blood products sparingly, although an absolute threshold for transfusion was not specified. RESULTS: Twenty-one of 192 patients (10.7%) developed an SSI in the pre-intervention period, whereas 1 of 84 patients (1.2%) developed an SSI in the post-intervention period (p=0.006). Surgical site infection was associated with obesity (a body mass index [BMI] ≥30) (11.5% vs. 4.8%, p=0.04), receipt of a blood transfusion (18.2% vs. 6.6%, p=0.03), and abdominal skin preparation with PI as opposed to CHG (10.1% vs. 2.0%, p=0.07). Chlorhexidine gluconate was used more commonly for abdominal skin preparation in the post- than in the pre-intervention period (6.6% pre-intervention vs. 50.7% post-intervention, p <0.0001). CONCLUSIONS: A multifaceted intervention decreased dramatically the rate of SSI after abdominal hysterectomy at our institution. No single component of the intervention could be identified as most responsible for the improvement.

The occurrence of preterm delivery is linked to pregnancy-specific distress and elevated inflammatory markers across gestation.

There is mounting evidence that stress during pregnancy can have detrimental effects on gestation and birth. Existing studies indicate that prenatal stress may increase levels of circulating inflammatory markers that are associated with prematurity and pregnancy complications, suggesting that stress-related changes in the cytokine milieu may increase the risk of poor pregnancy outcome. Previous studies, however, have not clearly connected stress during pregnancy to changes in inflammatory mediators and, in turn, to clinically-relevant outcomes such as premature delivery. The present study sought to directly connect prenatal stress and changes in inflammatory markers to preterm delivery and gestational age at birth (GAB). A sample of 173 women was recruited during the first trimester of pregnancy and followed through delivery. Overall stress, pregnancy-specific distress, and inflammatory markers were assessed early and later in pregnancy, and the predictive value of these measures for preterm birth and GAB was determined. There were significant differences in pregnancy-specific distress, IL-6, and TNF-α between women who delivered prematurely versus those who delivered at term, and elevated levels of pregnancy-specific distress, IL-6, and TNF-α were predictive of shortened GAB overall. Importantly, in many cases, the effects of overall stress and pregnancy-specific distress on GAB were mediated by levels of circulating inflammatory markers. Collectively, these data provide strong evidence that prenatal stress experiences can affect the timing of parturition via alterations in circulating inflammatory mediators, and underscore the need for ongoing research aimed at further understanding the mechanisms and effects of prenatal stress on maternal and infant health.

Beyond core measures: identifying modifiable risk factors for prevention of surgical site infection after elective total abdominal hysterectomy.

BACKGROUND: Despite adherence to the Centers for Medicare and Medicaid Services (CMS) core measures for preventing surgical site infections (SSI), our institution has a >10% rate of SSI after total abdominal hysterectomy (TAH), higher than the 90(th) percentile for SSI rates published in the 2009 National Healthcare Safety Network report. METHODS: A retrospective chart review was performed for patients who underwent elective TAH at a public safety net hospital in Denver from December 30, 2005, to March 9, 2010. The primary outcome was development of SSI within 30 days. A secondary outcome was adherence to CMS core measures. RESULTS: A total of 192 patients were included in the analysis, of whom 21 (10.9%) developed SSI. More than 95% had received antibiotics in the 60 min before surgical incision, and >90% received an appropriate antibiotic. Compliance with post-anesthesia care unit normothermia was equivalent in the SSI and non-SSI groups (81.0% vs. 75.2%; p=0.5588). Surgical site infection was associated with obesity (body mass index [BMI]≥30) (15.4% vs. 6.9%; p=0.0609), estimated blood loss≥500 mL (18.5% vs. 8.0%; p=0.0353), and receipt of a blood transfusion (28.6% vs. 10.5%; p=0.0183). In a multiple logistic regression model, obesity marginally increased the risk of SSI (odds ratio [OR] 2.55; 95% confidence interval [CI] 0.94-6.74), whereas blood transfusion was significantly associated with a higher risk of SSI (OR 3.58; 95% CI 1.21-10.62). CONCLUSIONS: Blood transfusion was associated with SSI after TAH in our population. As it is a modifiable risk factor, larger multi-center studies are needed to confirm this result and determine appropriate transfusion thresholds.

Disorders of sexual desire and arousal.

Desire and arousal disorders are very common. These disorders can cause significant distress to a patient. A successful approach depends on an accurate diagnosis, which is dependent on history. Laboratory evaluation is usually not helpful, whereas psychosexual therapy is helpful in many cases. Although there is some evidence that drug therapy is helpful in some cases, no drug has been approved for the treatment of these disorders.

Orgasmic dysfunction.

Orgasmic disorders are common in women. Unfortunately a lack of consistent, uniform definitions has made this a difficult disorder to study in depth. Etiology is frequently multifactorial, with psychologic issues often playing a prominent role. Diagnosis depends on a detailed history, which then guides treatment to target the underlying causes. Cognitive behavioral therapy has the most favorable outcome evidence to date.

Pharmacological effects on sexual function.

Many drugs may have effects on sexual function. Sexual function is complex and psychological and relationship issues are likely to have greater impacts on sexual function in women than drugs. Although it is important to understand the effects of drugs on sexual function, physicians should use caution in "medicalization" of sexual function in women [106].

Differences in inflammatory cytokine and Toll-like receptor genes and bacterial vaginosis in pregnancy.

OBJECTIVE: This study was undertaken to estimate the frequency of inflammatory cytokine and Toll-like receptor gene polymorphisms in women with and without bacterial vaginosis (BV) in pregnancy. STUDY DESIGN: A secondary analysis was performed of pregnant women at less than 30 weeks' gestation enrolled as part of 2 multicenter studies. Eight hundred eighty-five women were assessed for BV (defined as Nugent's vaginal Gram stain score 7-10 and a pH > 4.5). Comparisons were made between women with or without BV. Extracted maternal DNA was analyzed for 7 cytokine (interleukin [IL] 1beta-511, IL1beta Exon 5 +3954, IL6-174, IL8-845, IL10-1082, tumor necrosis factor alpha-238 [TNFalpha-238], TNFalpha-308) and 2 Toll-like receptor (TLR-4 299, TLR-4 399) gene polymorphisms. RESULTS: BV was diagnosed in 497 women and 388 did not have BV. Genotype and allele frequency analyses revealed associations with BV and polymorphisms at the IL1beta Exon 5 +3954, IL6-174, IL10-1082, and TLR-4 399 loci. Women with BV were less likely to be homozygous (C/C) for IL1beta Exon 5 +3954 (P = .04). Women with BV were also less likely to have polymorphisms at the IL10-1082 (P = .03) and TLR-4 399 (P = .04) loci in the univariate analysis. Women with BV were more likely to be heterozygous (G/C) for the IL6-174 genotype (P < .0001). Multivariate analysis, controlling for maternal race, confirmed the following associations with BV: IL1beta Exon 5 +3954 (odds Ratio [OR] 0.5, 95% CI 0.3-0.9) and IL6-174 (OR 2.2, 95% CI 1.6-3.1). In addition, polymorphism at the IL8-845 locus was associated with a decreased risk for BV (OR 0.6, 95% CI 0.4-1.0). CONCLUSION: After controlling for race, polymorphisms at the IL1beta Exon 5 +3954, IL6-174, and IL8-845 loci were associated with an altered rate of BV in pregnancy.

Systemic administration of betamethasone delays endotoxin-induced preterm labor in the murine model.

OBJECTIVE: The purpose of this study was to determine whether the administration of betamethasone decreases the endotoxin-induced preterm parturition rate and inhibits the risk of cytokines in the murine model. STUDY DESIGN: Endotoxin was administered intraperitoneally at gestational day 15 (75% of gestation). In phase I, the duration of gestation was measured in 36 gravid C3H/HeOu mice that were equally divided into four treatment groups: control, endotoxin only, and two different dose regimens of betamethasone followed by endotoxin. In phase II, maternal serum and amniotic fluid concentrations of cytokines (interleukin-1alpha, tumor necrosis factor-alpha, and interleukin-6) were measured at 4 hours after endotoxin injection in 44 gravid mice divided equally in the four treatment groups. RESULTS: The group that was exposed only to endotoxin was delivered at a significantly earlier gestational age compared with the control group (16.2 +/- 0.4 days vs 19.6 +/- 0.2 days; P <.01). The two groups that were pretreated with betamethasone before the endotoxin were delivered at gestational ages similar to the control group. There was a marked increase of tumor necrosis factor-alpha and interleukin-6 levels in amniotic fluid of mice that were treated with endotoxin only compared with the control group (P <.001). No difference in cytokine levels was found in those mice that were premedicated with betamethasone compared with the control group. CONCLUSION: Antenatal administration of betamethasone to mice delayed preterm parturition that was induced by endotoxin. Elevations of amniotic fluid cytokine concentrations that were observed with endotoxin were not observed with pretreatment with betamethasone.