Articles: sepsis.
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Clinical Trial Controlled Clinical Trial
Alterations in coagulation and fibrinolysis during sepsis.
Circulating levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2 plasmin inhibitor complex (PIC) in 49 septic patients (23 patients with organ dysfunction (OD), 26 without OD) and 11 postgastrectomy patients were measured to determine the significance of the coagulation-fibrinolytic systems in the development of OD. Tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1), and thrombomodulin were also measured. The mean level of TAT on the day when OD occurred was significantly higher compared with the maximum level of TAT in septic patients without OD (P < .01) or postoperative patients (P < .01). ⋯ Septic patients with OD showed higher levels of PAI-1 (P < .001) but not of t-PA. Thrombomodulin levels were significantly higher in the septic patients with OD compared with the others (P < .001). We conclude that suppression of the fibrinolytic system contributes to the imbalance between coagulation and fibrinolysis, and that this hypercoagulable millieu on the endothelial surface leads to the onset of OD.
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The role of isolated blood transfusion as a means toward improving oxygen transport was evaluated in 19 critically ill patients having sepsis syndrome as defined by standard criteria. ICU therapies were unchanged during transfusion and hemodynamic profiles with serum lactate levels were obtained before and after packed red blood cells were given. ⋯ Oxygen uptake failed to increase with transfusion, corresponding to increased arterial and mixed venous oxygen content. In the presence of sepsis, patients having oxygen delivery and uptake above normal without evidence of ischemia (normal lactate) will not increase oxygen consumption by raising the hemoglobin.
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Journal of anesthesia · Mar 1996
Alterations in the myocardial β-adrenergic system during experimental endotoxemia.
In this study to investigate whether β-adrenergic receptor systems in the heart are impaired during endotoxemia, we examined two models of septic shock in rats, each of which has a different time course for the shock state. Male Wistar rats were divided into two groups: (1) the LPS (lipopolysaccharide) iv group (Escherichia coli endotoxin 1.0 mg·kg(-1) iv bolus administration), and (2) the CLP (cecal ligation and puncture model) group. As a control group for each model, a 0.9% saline injection group and a sham-operated group were also prepared. ⋯ The alteration in hemodynamics of septic-shock rats observed in this study was linked to the change in heart β-receptor density rather than the change in plasma CA. These observations suggested that the alterations which occur in the β-receptor system during endotoxemia depend upon the model of animal sepsis that is employed, and the time course of the septic-shock state. These alterations in the β-adrenergic system are thought to cause myocardial dysfunction during endotoxemia.
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Journal of critical care · Mar 1996
Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome.
Elevated arterial lactate concentrations in patients with sepsis have been interpreted as evidence of peripheral, nonpulmonary tissue hypoxia. These patients often develop pulmonary failure manifested by the acute respiratory distress syndrome (ARDS). As the result of tissue hypoxia or inflammation, the lungs of patients with sepsis and ARDS may become a source of lactate release into the circulation. ⋯ The lungs of patients with sepsis and ARDS may produce lactate. Pulmonary lactate release correlates with the severity of lung injury. The contribution of pulmonary lactate release should be considered when interpreting arterial lactate concentration as an index of systemic hypoxia.
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Critical care medicine · Mar 1996
ReviewIs it time to reposition vasopressors and inotropes in sepsis?
To review the literature on the current use of vasopressors and inotropes in patients with sepsis and sepsis syndrome with respect to the choice of agent, therapeutic end points, and safe and effective doses to be used. To examine the available evidence that supports or refutes goal-directed therapy toward supranormal oxygen transport in optimizing the outcome of critically ill sepsis syndrome patients. ⋯ Insufficient evidence exists to support goal-directed therapy with vasopressors and inotropes in the treatment of sepsis syndrome. No definitive recommendations can be made about the superiority of a vasopressor or inotropic agent due to the lack of data. However, it may be that evaluation of vasopressors earlier in sepsis syndrome will yield more promising results. Large, comparative, controlled trials assessing mortality rate and development of multiple organ system dysfunction are needed.