16 Jan 12
Posted in ScvO2, Sepsis at 1:01 by Laci
By M Varpula, S Karlsson, E Ruokonen, V Pettilä
Intensive Care Med (2006) 32:1336–1343
Central venous oxygen saturation (ScvO2) in initial resuscitation is included in the Surviving Sepsis Campaign guidelines. ScvO2 monitoring has also been suggested to be comparable to mixed venous oxygen saturation (SvO2) for clinical purposes. The aim of our study was to assess the correlation and agreement of ScvO2 and SvO2 and compare ScvO2?SvO2 difference to lactate, oxygen-derived and hemodynamic parameters in early septic shock in ICU after initial resuscitation.
Design and setting
Prospective clinical study with 16 patients with septic shock at two university hospital ICUs. A dose of norepinephrine over 0.1ug/kg/min was required for inclusion.
Measurements and results
Five paired ScvO2 and SvO2 samples at 6-h intervals, altogether 72 samples, were collected during 24 h. The mean SvO2 was below the mean ScvO2 at all time points. Bias of difference was 4.2% and 95% limits of agreement ranged from 8.1% to 16.5%. The difference correlated significantly to CI and DO2.
Conclusion
The difference between paired ScvO2 and SvO2 varies highly. Therefore, SvO2 may not be estimated on the basis of ScvO2 in treatment of septic shock after resuscitation period in ICU.
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12 Oct 10
Posted in Heart failure/Cardiogenic shock, Sepsis at 15:34 by Laci
By S Zanotti-Cavazzoni, S Hollenberg
Current Opinion in Critical Care 2009;15:392-397
Severe sepsis and septic shock are among the most important causes of morbidity and mortality in patients admitted to the intensive care unit. The purpose of this review is to review current understanding of sepsis-induced cardiac dysfunction and discuss pertinent findings regarding its clinical presentation, underlying mechanisms of disease, and therapy. Recent findings: Cardiac dysfunction in sepsis is characterized by decreased contractility, impaired ventricular response to fluid therapy, and in some patients ventricular dilatation. Current data support a complex underlying physiopathology with a host of potential pathways leading to myocardial depression. Circulating factors such as cytokines (TNF-[alpha], IL-1[beta]), lysozyme c, endothelin-1 have direct inhibitory actions on myocyte contractility. Nitric oxide has a complex role in sepsis-induced cardiac dysfunction. Current data suggest a combination of deleterious and positive effects on the myocardium determined by the specific type of nitric oxide expressed. Recent studies have shown that mitochondrial dysfunction and apoptosis also play a role in the development of sepsis-induced cardiac dysfunction. Current treatment for sepsis-induced cardiac dysfunction is based on appropriate treatment for the infectious focus (antibiotics and source control) and hemodynamic support (fluids, vasopressors, and inotropes). Summary: Cardiac dysfunction is common in patients with severe sepsis and septic shock. Current understanding of the underlying mechanisms responsible is rapidly evolving and future novel therapeutic targets may be soon available. Present therapy for sepsis-induced cardiac dysfunction is based on treatment of underlying sepsis with antibiotics and hemodynamic support.
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18 Mar 10
Posted in Sepsis at 0:02 by Laci
By C Pierrakos and J-L Vincent
Critical Care 2010, 14:R15
Biomarkers can be useful for identifying or ruling out sepsis, identifying patients who may benefit from specific therapies or assessing the response to therapy.
Methods
We used an electronic search of the PubMed database using the key words “sepsis” and “biomarker” to identify clinical and experimental studies which evaluated a biomarker in sepsis.
Results
The search retrieved 3370 references covering 178 different biomarkers.
Conclusions
Many biomarkers have been evaluated for use in sepsis. Most of the biomarkers had been tested clinically, primarily as prognostic markers in sepsis; relatively few have been used for diagnosis. None has sufficient specificity or sensitivity to be routinely employed in clinical practice. PCT and CRP have been most widely used, but even these have limited ability to distinguish sepsis from other inflammatory conditions or to predict outcome.
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05 Jan 10
Posted in Sepsis at 0:05 by Laci
By M Tidswell, W Tillis, S LaRosa, M Lynn, A Wittek, R Kao, J Wheeler, J Gogate, S Opal, the Eritoran Sepsis Study Group
Crit Care Med 2010;38:72-83
Endotoxin is a potent stimulus of proinflammatory response and systemic coagulation in patients with severe sepsis. Endotoxin is a component of Gram-negative bacteria that triggers an innate immune response through Toll-like receptor 4 signaling pathways in myeloid cells. We evaluated safety and tolerability of two dose regimens of eritoran tetrasodium (E5564), a synthetic Toll-like receptor 4 antagonist, and explored whether it decreases 28-day mortality rate in subjects with severe sepsis.
Design
Prospective, randomized, double-blind, placebo-controlled, multicenter, ascending-dose phase II trial.
Setting
Adult intensive care units in the United States and Canada.
Patients
Three hundred adults within 12 hrs of recognition of severe sepsis, with Acute Physiology and Chronic Health Evaluation (APACHE) II-predicted risk of mortality between 20% and 80%.
Interventions
Intravenous eritoran tetrasodium (total dose of either 45 mg or 105 mg) or placebo administered every 12 hrs for 6 days.
Measurements and main results
Prevalence of adverse events was similar among subjects treated with 45 mg or 105 mg of eritoran tetrasodium or with placebo. For modified intent-to-treat subjects, 28-day all-cause mortality rates were 26.6% (eritoran tetrasodium 105 mg), 32.0% (eritoran tetrasodium 45 mg), and 33.3% in the placebo group. Mortality rate in the eritoran tetrasodium 105-mg group was not significantly different from placebo (p = .335). In prespecified subgroups, subjects at highest risk of mortality by APACHE II score quartile had a trend toward lower mortality rate in the eritoran tetrasodium 105-mg group (33.3% vs. 56.3% placebo group, p = .105). A trend toward a higher mortality rate was observed in subjects in the lowest APACHE II score quartile for the eritoran 105-mg group (12.0% vs. 0.0% placebo group, p = .083).
Conclusions
Eritoran tetrasodium treatment appears well tolerated. The observed trend toward a lower mortality rate at the 105-mg dose, in subjects with severe sepsis and high predicted risk of mortality, should be further investigated.
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