Agenesia de arterias cerebelosas postero-inferiores en adulto asintomático con malformación de Dandy Walker / Agenesis of posterior inferior cerebellar arteries in an asymptomatic adult with Dandy-Walker malformation

No disponible

Ventilator-associated pneumonia due to colistin susceptible-only microorganisms.

Acinetobacter spp. and Pseudomonas aeruginosa are common pathogens of ventilator-associated pneumonia (VAP). The presentation and outcome of VAP due to Acinetobacter spp. and P. aeruginosa susceptible to carbapenems (Carb-S; imipenem and/or meropenem) and to colistin only (Col-S) were compared in the present retrospective study in three intensive care units. A total of 61 episodes of VAP caused by Acinetobacter spp. or P. aeruginosa were studied, of which 30 isolates were Carb-S and 31 were Col-S. Demographics, worsening of renal function and mortality were not different. The univariate analysis showed that a later onset and a previous episode of VAP, prior antimicrobial therapy for >10 days and previous therapy with carbapenems during the present admission were more frequent in patients with Col-S strains. On multivariate analysis, prior antimicrobial therapy for >10 days and a previous episode of VAP remained significantly associated with Col-S VAP. Approximately 41% of the infections caused by Col-S isolates, but none of those due to Carb-S isolates, had received prior carbapenem therapy. Colistin-susceptible ventilator-associated pneumonia episodes can be effectively treated using colistin without significant renal dysfunction. This susceptibility pattern could be suspected in patients with a previous ventilator-associated pneumonia episode or prior antibiotic therapy for >10 days preceding the present ventilator-associated pneumonia episode.

Papel de la microcirculación en el desarrollo de la lesión pulmonar aguda inducida por la ventilación mecánica / Role of microvasculature in the development of acute lung injury induced by mechanical ventilation

La presión capilar pulmonar es uno de los determinantes de la formación de edema pulmonar y además favorece el desarrollo de lesión pulmonar inducida por la ventilación mecánica (VILI). En consecuencia, en los enfermos críticos sometidos a ventilación mecánica (VM), la determinación ajustada de la presión capilar cobra mayor relevancia. El flujo vascular también es un factor determinante de la lesión pulmonar aguda, cuyo incremento favorece una mayor lesión pulmonar. El aumento de estas variables fisiológicas determina un incremento del estrés mecánico sobre las células del endotelio capilar pulmonar, lo que puede inducir una respuesta inflamatoria endotelial y favorecer la aparición o el empeoramiento de la lesión pulmonar aguda. En consecuencia, reducir el estrés vascular pulmonar puede disminuir la lesión pulmonar aguda en modelos experimentales

Pulmonary wedge pressure is one of the determinants of pulmonary edema and in addition favors the development of pulmonary injury induced by mechanical ventilation (PIMV). Accordingly, in the critically ill patients subject to mechanical ventilation (MV), the precise determination of pulmonary wedge pressure gain in importance. Vascular flow is also a decisive factor in acute pulmonary injury, and its increase favors a more intense pulmonary injury. The increase of these physiological variables determines an increment in mechanical stress on the cells of pulmonary capillary endothelium, and this stress can induce an endothelial inflammatory response with appearance or worsening of acute pulmonary injury. Accordingly, reducing pulmonary vascular stress can diminish acute lung injury in experimental models