Impacto de la crisis económica argentina sobre la incidencia de infecciones y la evolución en la Unidad de Cuidados Intensivos / Impact of the economic crisis Argentina on the incidence of infections and the evolution in Intensive care unit

Introducción. La crisis económica argentina disminuyó la provisión adecuada de insumos en los hospitales públicos. Objetivos. 1) Evaluar si la reducción de insumos impactó en la evolución de los pacientes; 2) cuantificar la provisión de insumos durante los períodos precrisis (P1), crisis y poscrisis (P2); 3) evaluar la incidencia de infecciones durante los tres períodos. Materiales y métodos. Se evaluó la densidad de incidencia de las infecciones intrahospitalarias, la estadía en la Unidad de Terapia Intensiva y la mortalidad en los tres períodos. Los datos se presentan como media ± desviación estándar, mediana [IC 0,25-0,75] y porcentajes de acuerdo con su naturaleza. Las comparaciones se efectuaron con la prueba t o ji cuadrado. Se consideró significativo un valor p <0,05. Resultados. Durante la crisis, ingresaron pacientes con menos enfermedades preexistentes, permanecieron más días ventilados y aumentó significativamente el número de infecciones por paciente. En el período P2, se detectó una caída significativa del número de pacientes infectados con respecto a los dos períodos anteriores. En el período P1, no hubo diferencias entre la mortalidad de los infectados y de los no infectados (25% contra 33%, p = 0,31). Durante la crisis, la mortalidad de los no infectados fue menor (19% contra 40%, p = 0,0005). La provisión de insumos disminuyó durante la crisis. Las infecciones intrahospitalarias se incrementaron en forma absoluta y como densidad de incidencia durante la crisis, y descendieron en el período P2. Conclusión. Durante la crisis económica, se recortaron los gastos de insumos y aumentó el número de infecciones por paciente.(AU)

Introduction. The collapse of the Argentinean economy in 2001 caused a shortage of material resources in public hospitals. Objectives. 1) To evaluate whether the decrease of material resources affected the outcome of patients in the Intensive Care Unit; 2) to quantify the provision of resources received in the Intensive Care Unit during three periods: Pre-crisis (P1), crisis, and post-crisis (P2); 3) to evaluate the incidence of infections during the three periods. Materials and methods. We compared the incidence of nosocomial infec- incidence of nosocomial infections; Intensive Care Unit stay, and mortality in the three periods. Data are presented as media ± SD, median [IQ 0.25-0.75], and percentages according to their nature. Comparison were performed using t test and chi-squared test. A p value <.05 was considered significant. Results. During the crisis, patients with less co-morbidities were admitted, they spent more time on mechanical ventilation, and the number of infections per patient was higher. Instead, during P2, there was a significant reduction of patients infected in relation to P1 and the crisis period. In P1, mortality did not differ between infected versus non-infected patients (25% vs. 33%; p = 0.31). However, during the crisis, mortality in non-infected patients was lower (19% vs. 40%; p = 0.0005). In the crisis, provision of materials decreased. Nosocomial infections increased. The incidence of infections decreased during P2. Conclusion. Resource availability decreased significantly during the economic crisis with a marked increase in the incidence of infections in the Intensive Care Unit. (AU)

Evidence for the stability and cytochrome P450 specificity of the phenobarbital-induced reductive halothane-cytochrome P450 complex formed in rat hepatic microsomes.

The hypothesis that the reduced spectral halothane-cytochrome P450 complex formed in rat hepatic microsomes is a stable cytochrome P450 specific species was examined. Comparisons of the cytochrome P450 inducers, phenobarbital (PB), pregnenolone-16 alpha-carbonitrile (PCN) and beta-naphthoflavone (beta-NF) showed that PB was the most effective inducer of the halothane-cytochrome P450 complex and the cytochrome P450 which liberates the halothane metabolites, 2-chloro-1,1-difluoroethene (CDE) and 2-chloro-1,1,1-trifluoroethane (CTE). However, the ratio of CDE produced to quantity of complex was found to be reduced 70-77% in these microsomes. A large portion of total microsomal cytochrome P450 was destroyed upon halothane reduction (up to 39%), yet the complexed cytochrome P450, particularly in microsomes from PB-treated animals, was resistant to the irreversible inactivation mechanisms of halothane reduction. The effects of reductive halothane metabolism on subsequent warfarin metabolism showed that 7-hydroxywarfarin formation from either (R)- or (S)-warfarin in microsomes from PCN-treated, PB-treated or untreated rats was highly susceptible to irreversible inhibition. In microsomes from PB-treated, but not PCN or untreated rats, the formation of one warfarin metabolite, 4'-hydroxywarfarin from (R)-warfarin, could be shown to be increased when complex was eliminated by photodissociation. These results suggest that PB-B is preferentially bound as complex and resistant to inactivation because of complex stability, and that halothane reduction readily destroys the cytochrome P450 form, PB-C.

Metabolism of 2-chloro-1,1-difluoroethene to glyoxylic and glycolic acid in rat hepatic microsomes.

The complete metabolic fate of the volatile anesthetic halothane is unclear since 2-chloro-1,1-diflurorethene (CDE), a reductive halothane metabolite, is known to readily release inorganic fluoride upon oxidation by cytochrome P-450. This study sought to clarify the metabolism of CDE by determining its metabolites and the roles of induce cytochrome P-450 forms in its metabolism. Upon incubation of [14C]CDE with rat hepatic microsomes, two major radioactive products were found which accounted for greater than 94% of the total metabolites. These compounds were determined to be the nonhalogenated compounds, glyoxylic and glycolic acids, which were formed in a ratio of approximately 1 to 2 of glyoxylic to glycolic acid. No other radioactive metabolites could be detected. Following incubation of CDE with hepatic microsomes isolated from rats treated with cytochrome P-450 inducers, measurement of fluoride release showed that phenobarbital induced CDE metabolism to the greatest degree at high CDE levels, isoniazid was the most effective inducer at low CDE concentrations, and beta-naphthoflavone was ineffective as an inducer. These results suggest that CDE biotransformation primarily involves the generation of an epoxide intermediate, which undergoes mechanisms of decay leading to total dehalogenation of the molecule, and that this metabolism is preferentially carried out by the phenobarbital- and ethanol-inducible forms of cytochrome P-450.