Postoperative deep wound infection in adults after posterior lumbosacral spine fusion with instrumentation: incidence and management.

Summary: The authors reviewed 817 instrumented lumbosacral fusions in adults and found an incidence of 3.2% deep wound infections. The primary focus of this study was the management of these infections, with particular attention to whether the implants needed to be removed. A consulting infectious disease specialist indicated that an acute infection of a low back fusion wound could not be healed without removal of the metallic implants. This opinion was in contrast to the authors' daily experience and prompted this study. The authors identified and reviewed 817 cases of instrumented posterior lumbosacral arthrodeses in adults. A detailed analysis of any case with a deep wound infection was performed and yielded and infection rate of 3.2% (26 patients). Of these, 24 achieved a clean, closed wound without removal of instrumentation through a protocol of aggressive debridement and secondary closure. Instrumentation removal is not necessary to obtain a clean, closed wound using an aggressive approach with early diagnosis, vigorous debridement in the operative room under general anesthesia, delayed primary or secondary closure, and appropriate antibiotic coverage. Key Words: AdultWound infection-Instrumentation-Lumbosacral arthrodesis-Postoperative lumbosacral wound infection. Postoperative wound infection in spinal surgery can be a significant problem with resulting prolonged hospitalization, increased costs, and compromise of the desired outcome. Despite strict attention to operating room sterility and the use of prophylactic antibiotics, wound infections continue to occur. Considerable controversy also exists regarding the best method to manage the infection once it occurs, particularly whether the internal fixation device needs to be removed for the infection to be eradicated. This study was designed to address both the incidence of wound infection in instrumented adult lumbosacral arthrodeses and the results of treatment of the infection. The study was stimulated by the written opinion of an infectious disease consultant who stated that successful solution of this acute infection problem cannot be achieved unless the surgeon removes the metallic implants. MATERIALS AND METHODS Using the Twin Cities Spine Center computerized database, we identified 817 adult patients who had undergone an instrumented posterior lumbosacral arthrodesis between January 1980 and December 1994 at our center. There were 382 (47%) men and 435 (53%) women, whos

Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure

Background: Repeated apnoea events cause intermittent hypoxia (IH), which alters the function of various systems and produces free radicals and oxidative stress. Methods: We investigated hepatic oxidative stress in adult mice subjected to intermittent hypoxia, simulating sleep apnoea. Three groups were submitted to 21 days of IH (IH-21), 35 days of IH (IH-35), or 35 days of sham IH. We assessed the oxidative damage to lipids by TBARS and to DNA by comet assay; hepatic tissue inflammation was assessed in HE-stained slides. Antioxidants were gauged by catalase, superoxide dismutase, glutathione peroxidase activity and by total glutathione. Results: After IH-21, no significant change was observed in hepatic oxidative stress. After IH-35, significant oxidative stress, lipid peroxidation, DNA damage and reduction of endogenous antioxidants were detected. Conclusions: In an animal model of sleep apnoea, intermittent hypoxia causes liver damage due to oxidative stress after 35 days, but not after 21 days

Validação do método de graus-dia para estimar a data de diferenciação da panícula (DP) de cultivares de arroz irrigado no Rio Grande do Sul.

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Genotoxic, neurotoxic and neuroprotective activities of apomorphine and its oxidized derivative 8-oxo-apomorphine

Apomorphine is a dopamine receptor agonist proposed to be a neuroprotective agent in the treatment of patients with Parkinson's disease. Both in vivo and in vitro studies have shown that apomorphine displays both antioxidant and pro-oxidant actions, and might have either neuroprotective or neurotoxic effects on the central nervous system. Some of the neurotoxic effects of apomorphine are mediated by its oxidation derivatives. In the present review, we discuss recent studies from our laboratory in which the molecular, cellular and neurobehavioral effects of apomorphine and its oxidized derivative, 8-oxo-apomorphine-semiquinone (8-OASQ), were evaluated in different experimental models, i.e., in vitro genotoxicity in Salmonella/microsome assay and WP2 Mutoxitest, sensitivity assay in Saccharomyces cerevisiae, neurobehavioral procedures (inhibition avoidance task, open field behavior, and habituation) in rats, stereotyped behavior in mice, and Comet assay and oxidative stress analyses in mouse brain. Our results show that apomorphine and 8-OASQ induce differential mutagenic, neurochemical and neurobehavioral effects. 8-OASQ displays cytotoxic effects and oxidative and frameshift mutagenic activities, while apomorphine shows antimutagenic and antioxidant effects in vitro. 8-OASQ induces a significant increase of DNA damage in mouse brain tissue. Both apomorphine and 8-OASQ impair memory for aversive training in rats, although the two drugs showed a different dose-response pattern. 8-OASQ fails to induce stereotyped behaviors in mice. The implications of these findings are discussed in the light of evidence from studies by other groups. We propose that the neuroprotective and neurotoxic effects of dopamine agonists might be mediated, in part, by their oxidized metabolites