Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Pathophysiology of septic encephalopathy an unsolved puzzle. | Flierl et al. Critical Care 2010 14 165 http content 14 3 165 CRITICAL CARE COMMENTARY L__ Pathophysiology of septic encephalopathy -an unsolved puzzle Michael A Flierl1 Daniel Rittirsch2 Markus S Huber-Lang3 and Philip F Stahel1 4 See related research by van der Boogaard etal. http content 14 3 R81 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. Howver 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. The clinical study by van der Boogaard and colleagues recently published in Critical Care 1 was designed to unravel some of the open questions regarding the pathophysiology of septic encephalopathy. The authors mimicked inflammation-associated encephalopathy by induction of experimental endotoxemia using Escheria coli-derived lipopolysaccharides LPSs in 15 healthy young volunteers. Outcome parameters were serum levels of cytokines cortisol neuron specific enolase S100-P as well as electroencephalographic changes and cognitive function in comparison to a healthy cohort of ten control volunteers. Interestingly van der Boogaard and colleagues described that the endotoxin-induced cytokine storm Correspondence department of .
