Another limitation is that the use of hypotension as the defining criteria for septic shock in this patient group may be imperfect. MAP is at best a surrogate of inadequate selleck compound microvascular perfusion Inhibitors,Modulators,Libraries in shock. It does not directly capture microcirculatory perfusion and cellular injury that lead Inhibitors,Modulators,Libraries to organ dysfunction and death. None the less, other metabolic markers such as serum lactate and bicarbonate levels as well as severity of illness scores were incorporated into the model to help adjust for variations in shock severity. Despite these limitations of blood pressure monitoring, given its universal access and ease of Inhibitors,Modulators,Libraries use, it is the most relied upon clinical parameter for guiding therapy and will remain a mainstay in the treatment of septic shock for the foreseeable future.

Conclusion From this study, we conclude that markedly delayed initiation of vasopressor medications in patients with septic shock is modestly associated with increased organ failure risk and decreased survival. Substantial delays of vasopressor initiation are required to see these effects. Given the almost universal use of vasopressors Inhibitors,Modulators,Libraries in septic shock and the critical need for precise titration, further study of this area is warranted. Key messages Delays in initiation of vasopressor therapy following the first documentation of hypotension in septic shock is modestly associated with increased specific organ failure and mortality risk This increase in specific organ failure and mortality risk is entirely driven by the decile of patients with the greatest delays of 14 hours.

Vasopressor initiation delays are not associated with increased time on vasopressors or on mechanical ventilation among survivors Delay of initiation of appropriate antimicrobial, age, and APACHE II score Inhibitors,Modulators,Libraries are also independent correlates of mortality Introduction Selenium plays an essential role in the protection against lipid peroxidation, in regulating T cell activity, mediating the inflammatory response and aiding thyroid hormone metabolism. The biological effects of selenium are achieved by 25 selenoproteins, among which the most known are selenoprotein P, the glutathione peroxidases, thioredoxin reductases and iodothyronine deiodinases. Plasma selenium is predominantly associated with three proteins selenoprotein P, which comprises over 50% of plasma selenium, glutathione peroxidase and albumin, which accounts for 20 40% and 9% of plasma selenium, respectively. Plasma concentration reflects a very low part of body selenium as there is only 0. 2 mg selenium in plasma for 20 40 mg in the whole selleck MEK162 body. Decreased plasma concentrations during the acute phase response have been described in animal and clinical studies.