Our goal was to determine the relevant variables and patient phenotypes to predict sepsis outcomes. We performed an ancillary study concerning 119 patients from three intensive care units (ICUs) in septic shock at ICU admittance (T0). We de ned clinical worsening as having an increased Sequential Organ Failure Assessment (SOFA) score ≥ 1 48 hours after admission (ΔSOFA ≥ 1). We performed univariate and multivariate analyses according to 28-day mortality rate and ΔSOFA ≥ 1, and determined three patient phenotypes: safe, intermediate and poor. Persistence of the intermediate and poor phenotypes after T0 were de ned as poor outcomes. At T0, the multivariate analysis showed two variables associated with 28-day mortality rate: norepinephrine dose and serum lactate concentration. Regarding ΔSOFA ≥ 1, we identi ed three variables at T0: norepinephrine dose, serum lactate concentration and venous-to-arterial carbon dioxide partial pressure difference (P(v-a)CO 2 ). At T0, the three phenotypes (safe, intermediate, and poor) were distributed in 28 (24%), 70 (59%) and 21 (18%) patients, respectively.We thus suggested an algorithm featuring norepinephrine dose, serum lactate concentration and P(va)CO 2 to predict patient outcomes and obtained an area under the curve (AUC) of 74% (63-85%). In conclusion, our ndings underline that identifying relevant variables and phenotypes may help physicians recognize patient outcomes.
Our goal was to determine the relevant variables and patient phenotypes to predict sepsis outcomes. We performed an ancillary study concerning 119 patients from three intensive care units (ICUs) in septic shock at ICU admittance (T0). We defined clinical worsening as having an increased Sequential Organ Failure Assessment (SOFA) score ≥ 1 48 hours after admission (ΔSOFA ≥ 1). We performed univariate and multivariate analyses according to 28-day mortality rate and ΔSOFA ≥ 1, and determined three patient phenotypes: safe, intermediate and poor. Persistence of the intermediate and poor phenotypes after T0 were defined as poor outcomes. At T0, the multivariate analysis showed two variables associated with 28-day mortality rate: norepinephrine dose and serum lactate concentration. Regarding ΔSOFA ≥ 1, we identified three variables at T0: norepinephrine dose, serum lactate concentration and venous-to-arterial carbon dioxide partial pressure difference (P(v-a)CO2). At T0, the three phenotypes (safe, intermediate, and poor) were distributed in 28 (24%), 70 (59%) and 21 (18%) patients, respectively. We thus suggested an algorithm featuring norepinephrine dose, serum lactate concentration and P(v-a)CO2 to predict patient outcomes and obtained an area under the curve (AUC) of 74% (63–85%). In conclusion, our findings underline that identifying relevant variables and phenotypes may help physicians recognize patient outcomes.
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