Critical care : the official journal of the Critical Care Forum
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On one side, brain dysfunction is a poorly explored complication of sepsis. On the other side, brain dysfunction may actively contribute to the pathogenesis of sepsis. ⋯ Recent observations have confirmed that sepsis is associated with excessive brain inflammation and neuronal apoptosis which clinical relevance remains to be explored. In parallel, damage within autonomic nervous and neuroendocrine systems may contribute to sepsis induced organ dysfunction.
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Midazolam is used routinely to sedate patients in the intensive care unit (ICU). We suspected that midazolam over-sedation was occurring in the ICU of the Guy's and St. Thomas' Trust and that it could be difficult to differentiate this from underlying neurological damage. A sensitive assay for detecting midazolam and 1-hydroxymidazolam glucuronide (1-OHMG) in serum was developed and applied in the clinical setting. ⋯ These findings confirm that prolonged sedation after midazolam therapy should be considered in the differential diagnosis of neurological damage in the ICU. This can be reliably detected by the assay method described. The effects of midazolam/1-OHMG persist days after administration of midazolam has ceased. After prolonged sedation has been excluded in this patient group, it is highly likely that neurological damage has occurred.
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The cuff-leak test has been proposed as a simple method to predict the occurrence of post-extubation stridor. The test is performed by cuff deflation and measuring the expired tidal volume a few breaths later (VT). The leak is calculated as the difference between VT with and without a deflated cuff. However, because the cuff remains deflated throughout the respiratory cycle a volume of gas may also leak during inspiration and therefore this method (conventional) measures the total leak consisting of an inspiratory and expiratory component. The aims of this physiological study were, first, to examine the effects of various variables on total leak and, second, to compare the total leak with that obtained when the inspiratory component was eliminated, leaving only the expiratory leak. ⋯ We conclude that the cross-sectional area around the endotracheal tube is not the only determinant of the cuff-leak test. System compliance and inspiratory flow significantly affect the test, mainly through an effect on the inspiratory component of the total leak. The expiratory component is slightly influenced by respiratory system resistance.
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The clinical and economic consequences of the emergence of multidrug-resistant Gram-negative bacteria in the intensive care unit (ICU) setting, combined with the high mortality rate among patients with nosocomial pneumonia, have stimulated a search for alternative therapeutic options to treat such infections. The use of adjunctive therapy with aerosolized colistin represents one of these. There is extensive experience with use of aerosolized colistin by patients with cystic fibrosis, but there is a lack of data regarding the use of aerosolized colistin in patients without cystic fibrosis. ⋯ Aerosolized colistin may be a beneficial adjunctive treatment in the management of nosocomial pneumonia (ventilator associated or not) due to multidrug-resistant Gram-negative bacteria.
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Review
Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury.
Apoptosis, or programmed cell death, is a physiological form of cell death that is important for normal embryologic development and cell turnover in adult organisms. Cumulative evidence suggests that apoptosis can also be triggered in tissues without a high rate of cell turnover, including those within the central nervous system (CNS). ⋯ In the current review we summarize the growing evidence that apoptosis occurs after traumatic brain injury (TBI), from experimental models to humans. This includes the identification of apoptosis after TBI, initiators of apoptosis, key modulators of apoptosis such as the Bcl-2 family, key executioners of apoptosis such as the caspase family, final pathways of apoptosis, and potential therapeutic interventions for blocking neuronal apoptosis after TBI.