Progress in pediatric septic shock.docVIP

 PAGE \* MERGEFORMAT 11 Progress in pediatric septic shock Keywords:: septic shock Pediatrics Therapy In 1963, before the advent of Intensive Care Medicine, University of Minnesota reported 900 cases of suffering from Gram-negative bacteria in children with septic shock, the mortality rate of 97%. In 1996, the United States a body of 100 cases of sepsis associated with multiple organ failure in children, studies have shown that the overall mortality rate was 15%. Although the prognosis of septic shock has been a marked improvement, but in newborns and children, there are still relatively high morbidity and mortality. In this paper, the progress of their research are reviewed. 1 Pathogenesis Septic shock represents a host of the pathophysiology of systemic inflammation response to systemic inflammation are known to induce two types of induction agent is endotoxin (gram-negative bacterial cell wall lipopolysaccharide composition) and ultra-antigen 〔 including gram-positive bacteria Peptidoglycan / lipoteichoic acid complexes, exotoxin (such as toxic shock syndrome toxin-1, tSST-1, toxic shock syndrome toxin -1), and in mycobacteria and virus-related toxins〕 . Circulating endotoxin and macrophage-membrane protein and lipopolysaccharide receptor binding lead to cD14 activation and expression of inflammatory genes 〔 1〕 . Superantigen from time, after the usual antigen-presenting cells (aPC), and t-cell receptor (tCR) identification process triggered by the blood circulation in 30% of t lymphocyte activation. Activated inflammatory cells initiate a series of biochemical cascades and activate phospholipase a2, cyclooxygenase, complement, and other cytokines, in turn leading to prostaglandins, platelet-activating factor (pAF), leukotriene and cytokine elevated 〔 2〕 . Tumor necrosis factor-α (tNF-α ) and interleukin-1β (iL-1β ) synergistic role in promoting cascade of positive feedback, and cause fever, vasodilation, cardiovascular failure and lactic acidosis. Th