Pathophysiology of septic encephalopathy--an unsolved puzzle.
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.
Flierl
Michael A
MA
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
Rittirsch
Daniel
D
Huber-Lang
Markus S
MS
Stahel
Philip F
PF
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
D015415:Biomarkers