Steroids sepsis corticus

(NEJM 2008;358(2):125) Intensive Insulin Therapy and Pentastarch Resuscitation in Severe Sepsis Background The role of intensive insulin therapy in patients with severe sepsis is uncertain. Fluid resuscitation improves survival among patients with septic shock, but evidence is lacking to support the choice of either crystalloids or colloids. Methods In a multicenter, two-by-two factorial trial, we randomly assigned patients with severe sepsis to receive either intensive insulin therapy to maintain euglycemia or conventional insulin therapy and either 10% pentastarch, a low-molecular-weight hydroxyethyl starch (HES 200/), or modified Ringer’s lactate for fluid resuscitation. The rate of death at 28 days and the mean score for organ failure were coprimary end points. Results The trial was stopped early for safety reasons. Among 537 patients who could be evaluated, the mean morning blood glucose level was lower in the intensive-therapy group (112 mg per deciliter [ mmol per liter]) than in the conventional-therapy group (151 mg per deciliter [ mmol per liter], P ). However, at 28 days, there was no significant difference between the two groups in the rate of death or the mean score for organ failure. The rate of severe hypoglycemia (glucose level, 40 mg per deciliter [ mmol per liter]) was higher in the intensive-therapy group than in the conventional-therapy group (% vs. %, P ), as was the rate of serious adverse events (% vs. %, P=). HES therapy was associated with higher rates of acute renal failure and renal-replacement therapy than was Ringer’s lactate. Conclusions The use of intensive insulin therapy placed critically ill patients with sepsis at increased risk for serious adverse events related to hypoglycemia. As used in this study, HES was harmful, and its toxicity increased with accumulating doses. ( number, NCT00135473 [] .)

Because sepsis interferes with the normal distribution of systemic blood flow to organ systems, core organs may not receive appropriate oxygen delivery. The microcirculation is the key target organ for injury in patients with sepsis. A decrease in the number of functional capillaries leads to an inability to extract oxygen maximally; this inability is caused by intrinsic and extrinsic compression of capillaries and plugging of the capillary lumen by blood cells. Increased endothelial permeability leads to widespread tissue edema involving protein-rich fluid.

On a macroscopic level, sepsis progresses along a spectrum from infectious insult to septic shock and multiorgan dysfunction. 25  Septic shock is a form of distributive shock, manifested in patients by an increase in cardiac output and vasodilation. 24  The oxygen demand of end organs exceeds oxygen delivery, and with the cellular switch from aerobic to anaerobic metabolism, lactate is produced. 28  As oxygen demands remain unmatched, perfusion decreases leading to end organ failure. With each organ system failure, absolute mortality increases by 15%-20%. 27

The study's outcomes sharply contrasted those of the smaller but well designed Annane Trial . These differences are probably due to 1) the Annane Trial's population generally being more critically ill at study entry, 2) having a markedly higher mortality rate in the placebo group, and 3) enrollment occurring within 8 hours (vs. 72 hours in CORTICUS). Although the Annane Trial used hydrocortisone plus the pure mineralocorticoid fludrocortisone (while CORTICUS used hydrocortisone alone), the addition of fludrocortisone probably did not have a meaningful effect given that hydrocortisone doses of ≥200 mg/day maximally activate the mineralocorticoid receptor. Furthermore, a subsequent 2013 study by Boonen et al. [1] has called into question our current understanding of steroid metabolism during critical illness as they found a reduction of mediators of cortisol degradation in ICU patients. As such, conventional plasma measurements of the hormone may be inaccurate.

Steroids sepsis corticus

steroids sepsis corticus

The study's outcomes sharply contrasted those of the smaller but well designed Annane Trial . These differences are probably due to 1) the Annane Trial's population generally being more critically ill at study entry, 2) having a markedly higher mortality rate in the placebo group, and 3) enrollment occurring within 8 hours (vs. 72 hours in CORTICUS). Although the Annane Trial used hydrocortisone plus the pure mineralocorticoid fludrocortisone (while CORTICUS used hydrocortisone alone), the addition of fludrocortisone probably did not have a meaningful effect given that hydrocortisone doses of ≥200 mg/day maximally activate the mineralocorticoid receptor. Furthermore, a subsequent 2013 study by Boonen et al. [1] has called into question our current understanding of steroid metabolism during critical illness as they found a reduction of mediators of cortisol degradation in ICU patients. As such, conventional plasma measurements of the hormone may be inaccurate.

Media:

steroids sepsis corticussteroids sepsis corticussteroids sepsis corticus

http://buy-steroids.org