Prevención del Síndrome Confusional Agudo en pacientes ancianos hospitalizados con fractura de cadera

Introducción: Las consecuencias del síndrome confusional agudo en pacientes con fractura de cadera aumentan la morbilidad y la mortalidad de la persona, produciendo en numerosas ocasiones dependencia para el resto de su vida. El objetivo principal de esta revisión es la realización de un plan de actuación de enfermería, conociendo los factores de riesgo del delirium para la correcta prevención del mismo. Métodos: Se realiza una revisión bibliográfica en diferentes bases de datos para identificar cuáles son los factores predisponentes y precipitantes en ancianos hospitalizados con fractura de cadera susceptibles de padecer el síndrome confusional agudo. Resultados: No se han encontrado muchos artículos relacionados con la prevención no farmacológica del síndrome confusional agudo. A pesar de esto, las revisiones encontradas muestran que el delirium es una enfermedad prevenible mediante el conocimiento de los factores de riesgo y la correcta aplicación de cuidados de enfermería. En esta revisión se exponen los factores predisponentes y precipitantes del delirium y basado en diagnósticos NANDA, NOC y NIC se elabora un plan de cuidados para su prevención. Discusión: El delirium es una patología invalidante, pudiendo ser el precursor de la muerte de la persona, por lo que se le debe prestar la atención que merece. El anciano hospitalizado con fractura de cadera es un paciente de alto riesgo de padecerlo por todos los factores asociados que presenta. La prevención de factores de riesgo y el establecimiento de un plan de actuación son las medidas más útiles para evitar la aparición de esta enfermedad. En posteriores estudios de casos y controles se debería poner en práctica el plan de actuación realizado.

Changes in the Photoreceptor Mosaic of P23H-1 Rats During Retinal Degeneration: Implications for Rod-Cone Dependent Survival

Purpose. To investigate the spatiotemporal relationship between rod and cone degeneration in the P23H-1 rat. Methods. Control Sprague-Dawley (SD) and P23H-1 rats of ages ranging from P30 to P365 were used. Retinas were processed for whole mounts or cross sections and rods and cones were immunodetected. We used newly developed image analysis techniques to quantify the total population of L/M cones (the most abundant cones in the rat) and analyzed the rings of rod-cone degeneration. Results. In P23H-1 rats, rod degeneration occurs rapidly: first the rod outer segment shortens, at P30 there is extensive rod loss, and by P180 rod loss is almost complete except for the most peripheral retina. The numbers of L/M cones are, at all postnatal ages, lower in P23H-1 rats than in control SD rats, and decrease significantly with age (by P180). Rod and cone degeneration is spatiotemporally related and occurs in rings that appear already at P90 and spread throughout the entire retina. At P180, the rings of rod-cone degeneration are more abundant in the equatorial retina and are larger in the dorsal retina. Conclusions. This work describes for the first time that in the P23H-1 rat, rod and cone degeneration is spatiotemporally related and occurs in rings. Cone loss follows rod loss and starts very soon, even before P30, the first age analyzed here. The characteristics of the rings suggest that secondary cone degeneration is influenced by retinal position and/or other intrinsic or extrinsic factors.

Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a

Purpose: To study the population of intrinsically photosensitive retinal ganglion cells (melanopsin-expressing RGCs, m+RGCs) in P23H-1 rats, a rat model of inherited photoreceptor degeneration. Methods: At postnatal (P) times P30, P365, and P540, retinas from P23H dystrophic rats (line 1, rapid degeneration; and line 3, slow degeneration) and Sprague Dawley (SD) rats (control) were dissected as whole-mounts and immunodetected for melanopsin and/or Brn3a. The dendritic arborization of m+RGCs and the numbers of Brn3a+RGCs and m+RGCs were quantified and their retinal distribution and coexpression analyzed. Results: In SD rats, aging did not affect the population of Brn3a+RGCs or m+RGCs or the percentage that showed coexpression (0.27%). Young P23H-1 rats had a significantly lower number of Brn3a+RGCs and showed a further decline with age. The population of m+RGCs in young P23H-1 rats was similar to that found in SD rats and decreased by 22.6% and 28.2% at P365 and P540, respectively, similarly to the decrease of the Brn3a+RGCs. At these ages the m+RGCs showed a decrease of their dendritic arborization parameters, which was similar in both the P23H-1 and P23H-3 lines. The percentage of coexpression of Brn3a was, however, already significantly higher at P30 (3.31%) and increased significantly with age (10.65% at P540). Conclusions: Inherited photoreceptor degeneration was followed by secondary loss of Brn3a+RGCs and m+RGCs. Surviving m+RGCs showed decreased dendritic arborization parameters and increased coexpression of Brn3a and melanopsin, phenotypic and molecular changes that may represent an effort to resist degeneration and/or preferential survival of m+RGCs capable of synthesizing Brn3a.