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Panigada M.,Intensive Care and Emergency | Zacchetti L.,Intensive Care and Emergency | L'Acqua C.,Intensive Care and Emergency | Cressoni M.,Intensive Care and Emergency | And 6 more authors.
PLoS ONE | Year: 2015

Introduction: Impairment of fibrinolysis during sepsis is associated with worse outcome. Early identification of this condition could be of interest. The aim of this study was to evaluate whether a modified point-of-care viscoelastic hemostatic assay can detect sepsis-induced impairment of fibrinolysis and to correlate impaired fibrinolysis with morbidity and mortality. Methods: This single center observational prospective pilot study was performed in an adult Intensive Care Unit (ICU) of a tertiary academic hospital. Forty consecutive patients admitted to the ICU with severe sepsis or septic shock were included. Forty healthy individuals served as controls. We modified conventional kaolin activated thromboelastography (TEG) adding urokinase to improve assessment of fibrinolysis in real time (UK-TEG). TEG, UK-TEG, plasminogen activator inhibitor (PAI)-1, thrombin-activatable fibrinolysis inhibitor (TAFI), ddimer, DIC scores and morbidity (rated with the SOFA score) were measured upon ICU admission. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) of mortality at ICU discharge. Results: UK-TEG revealed a greater impairment of fibrinolysis in sepsis patients compared to healthy individuals confirmed by PAI-1. TAFI was not different between sepsis patients and healthy individuals. 18/40 sepsis patients had fibrinolysis impaired according to UK-TEG and showed higher SOFA score (8 (6-13) vs 5(4-7), p = 0.03), higher mortality (39% vs 5%, p = 0.01) and greater markers of cellular damage (lactate levels, LDH and bilirubin). Mortality at ICU discharge was predicted by the degree of fibrinolysis impairment measured by UK-TEG Ly30 (%) parameter (OR 0.95, 95% CI 0.93-0.98, p = 0.003). Conclusions: Sepsis-induced impairment of fibrinolysis detected at UK-TEG was associated with increased markers of cellular damage, morbidity and mortality. © 2015 Panigada et al.


Prisco L.,Intensive Care and Emergency | Iscra F.,Intensive Care and Emergency | Ganau M.,University of Trieste | Berlot G.,Intensive Care and Emergency
Journal of Neurosurgical Sciences | Year: 2012

Aim. Early hyperglycemia is a feature of traumatic brain injured (TBI) patients. The aim of our study was to analyze the impact of early hyperglycemia on inICU mortality in isolated TBI and its correlations with other factors responsible for secondary injury. Methods. We studied admission values (AV) and worse values in the first 48 hours (WV 48 h) of 112 ICU TBI patients (mortality 29-6%) of blood glucose (BG), base excess (BE), mean arterial pressure (MAP), PaO 2ZFiO 2 ratio and serum hemoglobin (Hb). Predictive strength as the area under the receiver operating curves (AUROC) and correlation between all variables were calculated. Results. Data are expressed as median, lst-3rd quartile. Both BG AV (147.5, 126-182 mg/dL; AUROC 0.716, P=0.0002) and WV 48 h (156.5,132-192 mg/dL; AUROC 0.721, P=0.0001) are predictive of mortality. AV and WV 48 h are respectively: PaO 2ZFiO 2 (366.8, 237.2-477.6 vs. 320, 214.4.426; P=0.05), MAP (90, 80-100.5 vs. 75, 66-83 mmHg; P<0.0001) and Hb (11.4, 9.7-13.1 vs. 10.6, 9-12.2 g/dL; P<0.02). BG AV and WV 48 h correlates with: age (r=0.419, P<0.0001 and r=0.489, P<0.0001), PaO 2ZFiO 2 AV (r -0.223, P<0.03 and r -0.236, P<0.02), PaO 2ZFiO 2 WV 48 h (r -0.215, P<0.03 and r -0.279, P<0.005) and MAP WV 48 h (r -0.216, P<0.03 and r -0.261, P<0.007). Conclusion. Early hyperglycemia is a major predictor of mortality and correlates with other factors responsible for secondary injury. Early hyperglycemia seems to be a marker of inflammatory reaction responsible for early cardiovascular and respiratory impairment.


PubMed | Intensive Care and Emergency, Epidemiology Unit, anchi Bonomi Hemophilia And Thrombosis Center and Coagulation Service and Thrombosis Research Unit
Type: Clinical Trial | Journal: PloS one | Year: 2015

Impairment of fibrinolysis during sepsis is associated with worse outcome. Early identification of this condition could be of interest. The aim of this study was to evaluate whether a modified point-of-care viscoelastic hemostatic assay can detect sepsis-induced impairment of fibrinolysis and to correlate impaired fibrinolysis with morbidity and mortality.This single center observational prospective pilot study was performed in an adult Intensive Care Unit (ICU) of a tertiary academic hospital. Forty consecutive patients admitted to the ICU with severe sepsis or septic shock were included. Forty healthy individuals served as controls. We modified conventional kaolin activated thromboelastography (TEG) adding urokinase to improve assessment of fibrinolysis in real time (UK-TEG). TEG, UK-TEG, plasminogen activator inhibitor (PAI)-1, thrombin-activatable fibrinolysis inhibitor (TAFI), d-dimer, DIC scores and morbidity (rated with the SOFA score) were measured upon ICU admission. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) of mortality at ICU discharge.UK-TEG revealed a greater impairment of fibrinolysis in sepsis patients compared to healthy individuals confirmed by PAI-1. TAFI was not different between sepsis patients and healthy individuals. 18/40 sepsis patients had fibrinolysis impaired according to UK-TEG and showed higher SOFA score (8 (6-13) vs 5 (4-7), p = 0.03), higher mortality (39% vs 5%, p = 0.01) and greater markers of cellular damage (lactate levels, LDH and bilirubin). Mortality at ICU discharge was predicted by the degree of fibrinolysis impairment measured by UK-TEG Ly30 (%) parameter (OR 0.95, 95% CI 0.93-0.98, p = 0.003).Sepsis-induced impairment of fibrinolysis detected at UK-TEG was associated with increased markers of cellular damage, morbidity and mortality.

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