Septic-associated encephalopathy - everything starts at a microlevel
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* Corresponding author: Tarek Sharshar tarek.sharshar@rpc.aphp.fr
1 Department of Intensive Care Medicine, Raymond Poincaré teaching Hospital and University of Versailles Saint-Quentin en Yvelines, 104 Boulevard Raymond Poincaré, 92380 Garches, France
2 Department of Anesthesiology Critical Care Medicine, Johns Hopkins University School of Medicine, Meyer 8-140, 600 N Wolfe St, Baltimore, MD 21287, USA
Critical Care 2010, 14:199 doi:10.1186/cc9254
See related research by Taccone et al., http://ccforum.com/content/14/4/R140
Published: 29 September 2010Abstract
Sepsis-associated encephalopathy is associated with increased mortality and morbidity. Its pathophysiology remains insufficiently elucidated, although there is evidence for a neuroinflammatory process sequentially involving endothelial activation, blood-brain barrier alteration and cellular dysfunction and alteration in neurotransmission. Experimental studies have shown that microcirculatory dysfunction, a consequence of endothelial activation, is an early pathogenic step. To date, we do not know whether it is present in septic patients, whether it accounts for clinical features and whether it is treatable.