Vaginal preparation with povidone iodine and postcesarean infectious morbidity: a randomized controlled trial.

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.

Clinical usefulness of white blood cell count after cesarean delivery.

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.

Cytotoxicity of oxidized low-density lipoprotein to mouse peritoneal macrophages: an ultrastructural study.

Mouse peritoneal macrophages (MPM) were incubated in culture medium containing low-density lipoprotein (LDL), oxidized LDL (oxLDL), or as controls, for 24 h. Scanning electron microscopy of MPM exposed to oxLDL showed loss of membrane ruffles and extensive plasmalemmal 'blebbing'. Transmission electron microscopy showed changes in up to 50 per cent of the cells, including vacuolation of the rough endoplasmic reticulum and reorganization of heterochromatin in the nuclei, characteristic of apoptosis. These changes were not seen in controls, nor in macrophages exposed to native LDL. Electron-dense crystals were found in the cytoplasm of 1 in 50 of cells exposed to oxLDL. These were found to have a high content of calcium and phosphorus. It is proposed that oxLDL is capable of inducing apoptosis, which might explain the origin of the necrotic base of advanced atherosclerotic plaques.

Fragmentation of DNA in P388D1 macrophages exposed to oxidised low-density lipoprotein.

Exposing a macrophage-like murine cell line to copper-oxidised low-density lipoprotein led to DNA fragmentation which was inhibited by the putative Ca2+/Mg2+ endonuclease inhibitor, zinc sulphate. DNA fragmentation preceded loss of membrane impermeability. These results suggest that apoptosis may be a mechanism of macrophage foam cell death in atherosclerotic lesions in the arterial wall.

Toxicity of oxidised low density lipoprotein towards mouse peritoneal macrophages in vitro.

The addition of cupric sulphate-oxidised low density lipoprotein (oxLDL) to mouse peritoneal macrophage (MPM) cultures caused toxicity towards the cells, measured by tritiated adenine release. The degree of toxicity increased with increasing concentrations of oxLDL up to 18 h incubation with MPM, after which the toxicity appeared to be independent of the concentration of oxLDL used. Toxicity was significantly reduced when vitamin E in the form of D,L-alpha-tocopherol was added to the LDL before the artificial oxidation, but vitamin E had no effect on the toxicity when added alongside the oxLDL in the culture medium. However, if the MPM were pre-incubated for 24 h with 80 microM vitamin E, there was a significant reduction in the level of toxicity up to 6 h in culture with oxLDL. There was a strong correlation (r = 0.81) between the degree of oxidation of the LDL, measured as thiobarbituric-reactive substances, and the corresponding toxicity. This indicated that the more oxidised the LDL was, the more toxic it was to the macrophages. Native LDL also led to toxicity, but only after a time-lag of 20 h. Again, this toxicity was decreased by pre-incubation of the MPM with vitamin E, but not by addition of vitamin E at the same time as LDL. The findings suggest that oxLDL is capable of contributing to the onset of necrosis during atherogenesis and that the oxidative capacity of the macrophage foam cells themselves might contribute to the process.

Cellular damage in mouse peritoneal macrophages exposed to cholesteryl linoleate.

Mouse peritoneal macrophages readily oxidize cholesteryl linoleate/bovine serum albumin emulsions to produce soluble lipid oxidation products, some of the latter being thought to cause cell damage. Mouse peritoneal macrophages were therefore incubated in the presence of cholesteryl linoleate/bovine serum albumin emulsion with and without the addition of dl-alpha tocopherol. The macrophages were observed morphologically and cell damage was estimated by three methods: trypan blue exclusion, lactate dehydrogenase release and tritiated adenine release. All the methods showed significant cell damage which was reduced in the presence of physiological levels of dl-alpha tocopherol. Cholesteryl oleate/bovine serum albumin, which is taken up by macrophages but is not oxidized, was not toxic. dl-Alpha tocopherol was itself toxic in higher concentrations. This self-inflicted macrophage damage might explain the onset of necrosis in atherosclerotic plaques.