RESUMO
This article provides an introduction to the definition of and rationale for outcomes management and includes a brief review of the outcomes management literature. A model for outcomes management, which links processes that can be changed in care delivery to outcomes that can be measured in a patient population, is reviewed. Guidelines for application of the outcomes management model and practical examples of application to two surgical patient populations are presented. Finally, issues important to outcomes management as a tool for performance improvement are discussed.
Assuntos
Ponte de Artéria Coronária/normas , Transplante de Rim/normas , Avaliação de Resultados em Cuidados de Saúde/métodos , Avaliação de Resultados em Cuidados de Saúde/organização & administração , Ponte de Artéria Coronária/enfermagem , Cardiopatias/enfermagem , Cardiopatias/cirurgia , Humanos , Nefropatias/enfermagem , Nefropatias/cirurgia , Transplante de Rim/enfermagem , Modelos OrganizacionaisRESUMO
The effect of degassing on the cytotoxicity of an ethylene oxide (EtO)-sterilized copolymer constituent of a bone replacement material, was determined using the (51)Cr release assay. An initial experiment used mouse L929 cells and a copolymer with an ambient pressure and temperature (APT) degassing time of 24 hr. Both copolymer and nylon control discs caused a significantly (P = 0.05) increased release of (51)Cr from the cells when compared with discs that had not been EtO sterilized. In a second experiment using L929 cells, copolymer and nylon discs were EtO-sterilized and degassed (APT) for 1-14 days. After 24 hr in culture, discs degassed for up to 14 days caused significantly increased cytotoxicity. A third experiment used L929 cells and copolymer/demineralized bone matrix blocks with APT degassing times of 2, 4 and 6 wk, or vacuum degassing for 48 hr. A decrease in cytotoxicity was observed from 2 to 6 wk of degassing, but there was still a significant increase over the untreated discs at 2 and 4 wk and a non-significant increase at 6 wk. Vacuum degassing was comparable to 4 wk of APT. In the fourth experiment, vacuum degassing times of 1, 7 and 14 days were studied using both L929 and human fibroblast cells. Vacuum degassing for up to 14 days did not reduce the cytotoxicity to the levels observed for samples that had not been EtO sterilized. All four experiments demonstrated that EtO sterilization of the copolymer used in bone replacement materials caused increased in vitro cytotoxicity compared with non-sterilized copolymer, and that degassing either at APT for up to 6 wk or vacuum degassing for up to 14 days reduced, but did not eliminate, the cytotoxicity observed.
RESUMO
Chlorphentermine HCl (CP) was used to induce preexisting alveolar alterations resembling a pulmonary lipidosis in mice to study these effects on the severity and duration of nitrogen dioxide (NO2) toxicity. Results indicated that a daily dose of 120 mg/kg for 14 days produced consistent histopathologic changes characterized by an accumulation of large foamy macrophages. Male Swiss-Webster mice were divided into a control and three treatment groups. Group 1 received 120 mg/kg CP po daily for 2 weeks followed by exposure to air for 48 hr. Group 2 received 20 ppm NO2 for 48 hr via whole-body inhalation, and group 3 received 120 mg/kg CP daily for 2 weeks followed by 20 ppm NO2 for 48 hr. The fourth group served as a nontreated control and received water in place of CP and air in place of NO2. All groups were compared by morphologic evaluation of pulmonary tissues at the light and electron microscopic levels at Days 0, 1, 3, 5, and 7 after the 48-hr exposure to air or NO2. In a second experiment using the same treatment groups, thin-section light microscopy was used to count the number of type I and type II cells and macrophages. NO2 exposure alone caused deaths in 20.8 and 18.5% of the mice in the two studies, but no deaths were seen in the combination groups from both experiments. Histopathologic evaluation showed a typical cellular response to the NO2 exposure, but differences were noted between the two groups receiving NO2 on this treatment. There was increased type II cell hyperplasia and terminal bronchiolitis on Days 0 and 1 but less on Days 3 to 7 in the combination group compared to the NO2 alone group. CP treatment prior to NO2 exposure caused less terminal bronchiolar epithelial hyperplasia and less pulmonary edema than was seen in the NO2 along group. The CP treatment appeared to protect against the lethal effects of NO2 at the concentration and time of exposure used and altered the cellular repair mechanism that occurs in response to NO2 toxicity. CP treatment prior to NO2 exposure caused significantly less loss of type I cells and less increase in type II cells due to NO2 damage. The combination treatment also caused an increase in macrophages greater than that seen in either individual treatment, and this number remained increased through 5 days post-NO2 exposure, whereas the NO2 alone caused a steady increase in macrophages following the exposure until Day 3.(ABSTRACT TRUNCATED AT 400 WORDS)
Assuntos
Clorfentermina/toxicidade , Pulmão/efeitos dos fármacos , Dióxido de Nitrogênio/toxicidade , Fentermina/análogos & derivados , Animais , Peso Corporal/efeitos dos fármacos , Contagem de Células , Hiperplasia , Lipidoses/induzido quimicamente , Pulmão/patologia , Pulmão/ultraestrutura , Macrófagos/efeitos dos fármacos , Macrófagos/patologia , Masculino , Camundongos , Microscopia EletrônicaRESUMO
Classification issues in ambulatory care nursing present an exciting area for future research and development that is only beginning to be tackled. It will be important to validate both the conceptual basis of the nursing workload model and the tools and methods used to measure workload. Comparative studies are needed in a variety of settings to reach consensus about the variables affecting workload in ambulatory nursing, and ways to measure them. Timed observation and validation studies are needed as new reporting and evaluation instruments are developed. At NIH a validation study looking at a modification of the taxonomy of ambulatory nursing practice (Verran, 1981) is underway, using a national sample of nursing administrators (Hastings, 1984). Studies to establish interrater reliability and to refine criteria for classifying patients and nursing activities are also needed.
Assuntos
Assistência Ambulatorial/classificação , Hospitais , Serviço Hospitalar de Enfermagem/classificação , Pacientes/classificação , Atividades Cotidianas , Coleta de Dados , Humanos , Maryland , Modelos Teóricos , National Institutes of Health (U.S.) , Análise e Desempenho de Tarefas , Estados UnidosRESUMO
Ambulatory care is a rapidly growing sector of health care that presents both a challenge and an opportunity for nursing administration. This article presents a quality assurance model that can be used to define and measure quality in ambulatory nursing services. Evaluation factors, tools, and methods are described. This program was designed and could be replicated by a nurse manager and staff at the unit level.
Assuntos
Assistência Ambulatorial/normas , Auditoria de Enfermagem/métodos , Cuidados de Enfermagem/normas , Garantia da Qualidade dos Cuidados de Saúde , Comportamento do Consumidor , Objetivos , Humanos , Maryland , Modelos Teóricos , Ambulatório Hospitalar , Admissão e Escalonamento de Pessoal/normas , Recursos HumanosRESUMO
Male, weanling Syrian hamsters (Mesocricetus auratus) were given (for 10 weeks) diets supplemented with manganese sulfate, aflatoxin, or a combination of both. All animals were killed and a histopathologic evaluation was performed on each liver to assess the influence of a manganese-supplemented diet on aflatoxicosis. Serum cholesterol and liver glycogen levels were also analyzed to further study the interaction of manganese and aflatoxin. Characteristic aflatoxin-induced precancerous histopathologic changes were observed in animals receiving the toxin. These changes included bile duct cell hyperplasia, enlarged nuclei, nuclear inclusions, and megala-hepatocytes. The dietary manganese addition to aflatoxin animals caused a slight reduction in the bile duct cell hyperplasia and significantly reduced the enlarged nuclei and nuclear inclusions. The latter indicates that the manganese may be influencing membrane chemistry. Animals receiving aflatoxin alone showed significantly increased serum cholesterol and liver glycogen. The cholesterol levels were significantly increased over the aflatoxin-induced levels when manganese was given in combination with the aflatoxin. The manganese lowered the increased liver glycogen levels caused by the aflatoxin. Dietary manganese shows some potential in suppressing several, but not all, of the aspects of developing aflatoxicosis in the hamster. The specific mode and site of action of manganese requires additional study.