Sparing brain damage in severe sepsis a beginning 英文参考文献.docVIP

Young Critical Care 2010,14:159 /content/14/3/159 COMMENTARY Sparing brain damage in severe sepsis: a beginning G Bryan Young* See related research by Spapen et al., /content/14/2/R54 other more reversible mechanisms of SAE, for example, Abstract neurotransmitter imbalances from altered amino acid ratios in the blood, dysfunction of other organs, transient alterations in blood-brain barrier function, slow clear- ance of sedative drugs, or only mild alterations in brain perfusion [7]. More advanced cases of sepsis and SAE may have neuron-killing complications: microcirculatory disturbances, excitotoxicity, oxidative stress and apop- totic mechanisms that also a? ect other organs [6]. Many of these complications are thought to arise from cytokine-mediated e? ects, either directly or indirectly acting on the microvasculature, coagulation system or on the organs themselves [8]. Sepsis-associated encephalopathy (SAE) resembles metabolic encephalopathies but with a di?erence: there is the potential for enduring brain damage/ dysfunction. The pathogenesis of SAE is likely multifactorial. However, the severity of SAE parallels the severity of the septic illness and the brain’s microcirculation is probably a?ected in a similar manner to that of other organs. Mild cases of SAE are often completely reversible, but there is increasing evidence that severe cases have neurological sequelae. A better understanding of the mechanisms may lead to brain-sparing, protective strategies. Until now there is no recognized treatment for SAE, other than to treat the systemic illness and hope that the brain will recover along with the other organs. However, Spapen and colleagues in a recent issue of Critical Care the study by Spapen and colleagues [1] o? ers some hope that the brain can be helped and protected in SAE. e e brain is one of the ? rst authors conducted a trial in which patien