Abstract
Ventilator-associated pneumonia is a familiar foe in intensive care units, but those associated with Pseudomonas aeruginosa have a particularly adverse impact on outcome. Correct antibiotic therapy and a novel endotracheal tube may reduce this burden. Does activated protein C improve outcome from acute lung injury and what is the role played by hyperventilation therapy in traumatic brain injury? Recent research has attempted to answer these questions. Further novel approaches have been evaluated in the management of ischaemic heart disease, and more light has been shed on acute bowel injury.
Highlights
Ventilator-associated pneumonia (VAP) is strongly associated with adverse outcomes in mechanically ventilated patients in the intensive care unit (ICU)
The objective was to identify predictors of 30-day mortality and hospital costs in patients with VAP attributed to potentially antibiotic-resistant Gramnegative bacteria (Pseudomonas aeruginosa, Acinetobacter spp. and Stenotrophomonas maltophilia)
Patients receiving their first dose of appropriate antibiotic therapy within 24 hours of bronchoalveolar lavage (BAL) sampling had a statistically lower 30-day mortality rate and hospitalization cost as compared with patients receiving their first dose of appropriate therapy more than 24 hours after BAL (17.2% versus 50.0%)
Summary
Neumann and coworkers reported data from the BrainIT database concerning use of hyperventilation strategies and adherence to Brain Trauma Foundation Guidelines after traumatic brain injury (TBI) in intensive care medicine [9]. This was a retrospective study of monitoring data from 22 European centres and involved 151 patients. The latest editions of the Brain Trauma Foundation Guidelines maintain a restricted use of hyperventilation for the treatment of TBI because of its negative impact on cerebral blood flow/ oxygenation and clinical outcome [10,11]. The authors suggest that, in the absence of elevated intracranial pressure, hyperventilation is better avoided; and that intentional reduction in arterial carbon dioxide tension to below 35 mmHg has little supporting evidence
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