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Commentary

Pathophysiology of septic encephalopathy - an unsolved puzzle

Michael A Flierl1*, Daniel Rittirsch2, Markus S Huber-Lang3 and Philip F Stahel14

Author Affiliations

1 Department of Orthopaedic Surgery, University of Colorado School of Medicine, Denver Health Medical Center, 777 Bannock Street, Denver, CO 80204, USA

2 Division of Trauma Surgery, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland

3 Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, University Hospital Ulm, University of Ulm Medical School, Steinhövelstrasse 9, 89075 Ulm, Germany

4 Department of Neurosurgery, University of Colorado School of Medicine, Denver Health Medical Center, 777 Bannock Street, Denver, CO 80204, USA

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Critical Care 2010, 14:165  doi:10.1186/cc9035


See related research by van den Boogaard et al., http://ccforum.com/content/14/3/R81

Published: 16 June 2010

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.