Biomarkers of disordered coagulation and fibrinolysis in acute lung injury and acute respiratory distress syndrome

Comparison of plasma levels of biomarkers of disordered coagulation and fibrinolysis in 50 patients with acute lung injury and acute respiratory distress syndrome ventilated with low-tidal-volume ventilation. Plasma levels of protein C were significantly lower in nonsurvivors compared with survivors. Plasma levels of thrombomodulin were significantly higher in nonsurvivors compared with survivors. Plasma levels of plasminogen activator inhibitor 1 (PAI-1) were significantly higher in nonsurvivors compared with survivors. Data shown as boxplots: horizontal line, median; box, 25th to 75th percentiles; error bars, 10th to 90th percentiles. *= 0.0003, **= 0.005 and = 0.01 compared with survivors, Mann–Whitney U test.<p><b>Copyright information:</b></p><p>Taken from "Biomarkers of inflammation, coagulation and fibrinolysis predict mortality in acute lung injury"</p><p>http://ccforum.com/content/12/2/R41</p><p>Critical Care 2008;12(2):R41-R41.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2447583.</p><p></p

Biomarkers of inflammation in acute lung injury and acute respiratory distress syndrome

Comparison of plasma levels of biomarkers of inflammation in 50 patients with acute lung injury and acute respiratory distress syndrome ventilated with low-tidal-volume ventilation. Plasma levels of IL-8 and soluble intercellular adhesion molecule 1 (sICAM-1) were significantly higher in nonsurvivors than in survivors. Data shown as boxplots: horizontal line, median; box, 25th to 75th percentiles; error bars, 10th to 90th percentiles. *= 0.002 and **= 0.006 compared with survivors, Mann–Whitney U test.<p><b>Copyright information:</b></p><p>Taken from "Biomarkers of inflammation, coagulation and fibrinolysis predict mortality in acute lung injury"</p><p>http://ccforum.com/content/12/2/R41</p><p>Critical Care 2008;12(2):R41-R41.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2447583.</p><p></p

Additional file 1 of Rapidly improving ARDS differs clinically and biologically from persistent ARDS

Additional file 1. Figure E1. Study Design. All patients were enrolled in the Early Assessment of Renal and Lung Injury (EARLI) cohort from November 2008 to May 2018. We analyzed data from 215 patients who met Berlin criteria for ARDS on day 1 or 2 of the study, were endotracheally intubated at the time of meeting Berlin criteria, and had plasma biomarker measurements available. Patients met criteria for rapidly improving ARDS if any of the following criteria were met: (i) Pao2:Fio2 > 300 or (ii) Spo2:Fio2 > 315 on the day following diagnosis of ARDS (day 2) or (iii) unassisted breathing by day 2 and for the next 48 hours (defined as absence of endotracheal intubate on day 2 through day 4). Table E1. Comorbidities were compared in patients with RIARDS versus persistent ARDS. Cirrhosis was more commonly identified in persistent ARDS. Other comorbidities were not significantly different between each group. Table E2. Concomitant medical conditions were compared in patients with RIARDS versus persistent ARDS. Hypertensive crisis at time of enrollment was more common in patients with RIARDS compared to those with persistent ARDS. Table E3. Type of steroids administered over the first 48 hours of ARDS diagnosis in patients with RIARDS compared to those with persistent ARDS. Table E4. Sensitivity analysis focused on patients with severe ARDS (defined by a PaO2:FiO2 equal to or less than 100 at time of enrollment). Vasopressor-dependent shock was more commonly seen in patients with severe persistent ARDS compared to severe RIARDS. Hospital mortality was significantly higher while ICU-free days was lower in those with severe persistent ARDS compared to severe RIARDS. Table E5. Sensitivity analysis focused on patients with severe ARDS. Patient comorbidities did not differ significantly between RIARDS and persistent disease among those with severe ARDS. Table E6. Sensitivity analysis focused on patients with severe ARDS. Concomitant medical conditions did not differ significantly between RIARDS and persistent disease among those with severe ARDS. Table E7. Sensitivity analysis focused on patients with severe ARDS. Ventilatory parameters did not differ significantly between RIARDS and persistent disease among those with severe ARDS. Table E8. Sensitivity analysis focused on patients with severe ARDS (defined by a PaO2:FiO2 equal to or less than 100 at time of enrollment). Plasma inflammatory biomarkers were significantly higher in those with severe persistent ARDS compared to severe RIARDS. Table E9. Sensitivity analysis comparing RIARDS and persistent disease among cases allocated to the hyperinflammatory phenotype. Similar to the results seen in the overall cohort, compared to patients with hyperinflammatory persistent ARDS, patients with hyperinflammatory RIARDS had significantly lower in-hospital mortality at 28 days and higher ICU-free days. However, contrary to results seen in the overall cohort, vasopressor-dependent shock on day 1 was equally prevalent. Severe hypoxemia was more commonly seen in persistent ARDS and not appreciated in RIARDS. Table E10. Sensitivity analysis comparing RIARDS and persistent disease among cases allocated to the hyperinflammatory phenotype. Microbiology and medications received did not differ between each group. Table E11. Sensitivity analysis comparing RIARDS and persistent disease among cases allocated to the hyperinflammatory phenotype. No significant differences were found in plasma inflammatory biomarker concentration between patients with RIARDS and persistent ARDS. Table E12. Total counts of missing values. Ventilatory parameters stratified by persistent ARDS versus RIARDS. Table E13. Total counts of missing values. Biomarkers stratified by persistent ARDS versus RIARDS. Table E14. Total counts of missing values. Comorbidities and concomitant medical conditions stratified by persistent ARDS versus RIARDS