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: Septic-associated encephalopathy - everything starts at a microlevel. | Sharshar et al. Critical Care 2010 14 199 http content 14 5 199 c CRITICAL CARE COMMENTARY Open Access Septic-associated encephalopathy - everything starts at a microlevel 1 1 1 2 Tarek Sharshar Andrea Polito Anthony Checinski Robert D Stevens See related research by Taccone et al. http eontent 14 4 R140 Abstract 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. The experimental study by Taccone and colleagues recently published in Critical Care 1 aims to determine whether sepsis is associated with early cerebral micro-circulatory failure which is believed to play a role in the pathophysiology of sepsis-associated encephalopathy SAE . SAE is a frequent and severe complication of sepsis as it is associated with increased mortality morbidity and plausibly with diminished long-term cognitive performance 2 3 . Evidence suggests that SAE results from an alteration of neurotransmission the mechanisms of which are insufficiently elucidated. One pathophysiologic scenario is an inflammatory process that starts by cerebral endothelial activation 3 which directly releases or through alteration of the blood-brain barrier facilitates the passage of inflammatory mediators that is cytokines chemokines into the parenchyma. Increased permeability of the blood-brain barrier has been extensively documented in experimental models of sepsis has been linked to complement activation 4 and has been observed in septic
