Calculating Route: Functional Trajectories and Long-Term Outcomes in Survivors of Severe COVID-19.

OBJECTIVES: We investigated functional trajectories after severe COVID-19 and estimated their associations with adverse outcomes (falls, rehospitalizations, institutionalization, or death), cognition and post COVID-19 condition within 1-year of hospital discharge. DESIGN: Prospective cohort study. SETTING: A large academic medical center in Sao Paulo, Brazil. PARTICIPANTS: Survivors of COVID-19 admissions to an intensive care unit. INTERVENTIONS: None. MEASUREMENTS: We evaluated participants' disability status before hospital admission and three, six, nine, and twelve months after discharge using 15 activities of daily living. During follow-up, cognition and post COVID-19 condition (defined as persistent symptoms with duration ≥2 months) were assessed. A latent class growth analysis was performed to investigate functional trajectories after discharge. RESULTS: We included 422 participants (median age 63 years, 13.5% were frail before COVID-19). Four distinct functional trajectories could be identified: "minimal disability trajectory" (37.4% of participants), "mild disability trajectory" (37.9%), "moderate disability trajectory" (16.8%), and "severe disability trajectory" (7.8%). Compared with minimal disability trajectory, the odds ratios (95% confidence interval) for 1-year adverse outcomes were 2.28 (1.38-3.76) for minor disability trajectory; 4.21 (2.10-8.42) for moderate disability trajectory; and 4.16 (1.51-11.46) for severe disability trajectory, even after adjustments. The occurrence of post COVID-19 condition was 67.5% and associated with functional trajectories (p=0.004). Cognition was also associated with functional trajectories. CONCLUSION: Severe COVID-19 survivors can experience diverse functional trajectories, with those presenting higher levels of disability at increased risk for long-term adverse outcomes. Further investigations are essential to confirm our findings and assess the effectiveness of rehabilitation interventions, aiming to improve health outcomes in those who survived severe COVID-19 and other causes of sepsis.

Clinical utility of standard base excess in the diagnosis and interpretation of metabolic acidosis in critically ill patients

The aims of this study were to determine whether standard base excess (SBE) is a useful diagnostic tool for metabolic acidosis, whether metabolic acidosis is clinically relevant in daily evaluation of critically ill patients, and to identify the most robust acid-base determinants of SBE. Thirty-one critically ill patients were enrolled. Arterial blood samples were drawn at admission and 24 h later. SBE, as calculated by Van Slyke's (SBE VS) or Wooten's (SBE W) equations, accurately diagnosed metabolic acidosis (AUC = 0.867, 95 percentCI = 0.690-1.043 and AUC = 0.817, 95 percentCI = 0.634-0.999, respectively). SBE VS was weakly correlated with total SOFA (r = -0.454, P < 0.001) and was similar to SBE W (r = -0.482, P < 0.001). All acid-base variables were categorized as SBE VS <-2 mEq/L or SBE VS <-5 mEq/L. SBE VS <-2 mEq/L was better able to identify strong ion gap acidosis than SBE VS <-5 mEq/L; there were no significant differences regarding other variables. To demonstrate unmeasured anions, anion gap (AG) corrected for albumin (AG A) was superior to AG corrected for albumin and phosphate (AG A+P) when strong ion gap was used as the standard method. Mathematical modeling showed that albumin level, apparent strong ion difference, AG A, and lactate concentration explained SBE VS variations with an R² = 0.954. SBE VS with a cut-off value of <-2 mEq/L was the best tool to diagnose clinically relevant metabolic acidosis. To analyze the components of SBE VS shifts at the bedside, AG A, apparent strong ion difference, albumin level, and lactate concentration are easily measurable variables that best represent the partitioning of acid-base derangements.

Clinical utility of standard base excess in the diagnosis and interpretation of metabolic acidosis in critically ill patients.

The aims of this study were to determine whether standard base excess (SBE) is a useful diagnostic tool for metabolic acidosis, whether metabolic acidosis is clinically relevant in daily evaluation of critically ill patients, and to identify the most robust acid-base determinants of SBE. Thirty-one critically ill patients were enrolled. Arterial blood samples were drawn at admission and 24 h later. SBE, as calculated by Van Slyke's (SBE VS) or Wooten's (SBE W) equations, accurately diagnosed metabolic acidosis (AUC = 0.867, 95%CI = 0.690-1.043 and AUC = 0.817, 95%CI = 0.634-0.999, respectively). SBE VS was weakly correlated with total SOFA (r = -0.454, P < 0.001) and was similar to SBE W (r = -0.482, P < 0.001). All acid-base variables were categorized as SBE VS <-2 mEq/L or SBE VS <-5 mEq/L. SBE VS <-2 mEq/L was better able to identify strong ion gap acidosis than SBE VS <-5 mEq/L; there were no significant differences regarding other variables. To demonstrate unmeasured anions, anion gap (AG) corrected for albumin (AG A) was superior to AG corrected for albumin and phosphate (AG A+P) when strong ion gap was used as the standard method. Mathematical modeling showed that albumin level, apparent strong ion difference, AG A, and lactate concentration explained SBE VS variations with an R(2) = 0.954. SBE VS with a cut-off value of <-2 mEq/L was the best tool to diagnose clinically relevant metabolic acidosis. To analyze the components of SBE VS shifts at the bedside, AG A, apparent strong ion difference, albumin level, and lactate concentration are easily measurable variables that best represent the partitioning of acid-base derangements.