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In sepsis

Pixley RA, Colman RW (1997) The kallikrein-kinin system in sepsis syndrome. In Farmer SG (ed) Handbook of immunopharmacology - the kinin system. Academic Press, New York, pp 173-186... [Pg.676]

The inflammatory process in sepsis is linked to the coagulation system. Pro-inflammatory mediators maybe procoagulant and antifibrinolytic, whereas anti-inflammatory mediators may be fibrinolytic. A key factor in the inflammation of sepsis is activated protein C, which enhances fibrinolysis and inhibits inflammation. Protein C levels are decreased in septic patients. [Pg.1186]

Biomarkers of sepsis have been controversial. The routine use of endotoxin, procalcitonin, or other markers is not routinely recommend. Concentrations of procalcitonin in serum are usually increased in sepsis, but fail to differentiate between infection and inflammation. However, procalcitonin has a high negative predictive value and could allow for the discontinuation of antibiotics. [Pg.1188]

Appropriate empiric anti-infective therapy decreases 28-day mortality compared to inappropriate empiric therapy (24% versus 39%).22 23,30 Additionally, appropriate therapy administered within 1 hour of sepsis recognition also decreases complications and mortality.22-23,30 Empiric anti-infective therapy should include one, two, or three drugs, depending on the site of infection and causative pathogens (Table 79-3). Anti-infective clinical trials in sepsis and septic shock patients are scarce and have not demonstrated differences among agents therefore, factors that determine selection are ... [Pg.1190]


See other pages where In sepsis is mentioned: [Pg.676]    [Pg.1187]   
See also in sourсe #XX -- [ Pg.490 , Pg.490 , Pg.491 ]

See also in sourсe #XX -- [ Pg.490 , Pg.490 , Pg.491 ]




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