title: Pathophysiology of septic encephalopathy--an unsolved puzzle.
abstract: The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population.
authors.affiliation: Department of Orthopaedic Surgery, University of Colorado School of Medicine, Denver Health Medical Center, 777 Bannock Street, Denver, CO 80204, USA. michael.flierl@dhha.org
authors.forename: Michael A
authors.initials: MA
authors.lastname: Flierl
authors.forename: Daniel
authors.initials: D
authors.lastname: Rittirsch
authors.forename: Markus S
authors.initials: MS
authors.lastname: Huber-Lang
authors.forename: Philip F
authors.initials: PF
authors.lastname: Stahel
mesh_terms: D015415:Biomarkers; D001812:Blood-Brain Barrier / Q000382:microbiology*; D020806:Central Nervous System Bacterial Infections / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D003422:Critical Care; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology*; D008833:Microcirculation; D018805:Sepsis / Q000150:complications* / Q000276:immunology / Q000503:physiopathology
chemical_list: D015415:Biomarkers