Invasive Pneumococcal Disease and Long-Term Mortality Rates in Adults, Alberta, Canada.

The relationship between increased short-term mortality rates after invasive pneumococcal disease (IPD) has been frequently studied. However, the relationship between IPD and long-term mortality rates is unknown. IPD patients in Alberta, Canada, had clinical data collected that were linked to administrative databases. We used Cox proportional hazards modeling, and the primary outcome was time to all-cause deaths. First IPD events were identified in 4,522 patients, who had a median follow-up of 3.2 years (interquartile range 0.8‒9.1 years). Overall all-cause mortality rates were consistently higher among cases than controls at 30 days (adjusted hazard ratio [aHR] 3.75, 95% CI 3.29-4.28), 30‒90 days (aHR 1.56, 95% CI 1.27‒1.93), and >90 days (aHR 1.43, 95% CI 1.33-1.54). IPD increases risk for short, intermediate, and long-term mortality rates regardless of age, sex, or concurrent conditions. These findings can help clinicians focus on postdischarge patient plans to limit long-term effects after acute IPD infection.

Invasive pneumococcal disease and long-term outcomes in children: A 20-year population cohort study.

Background: Although vaccination against Streptococcus pneumoniae infections (such as invasive pneumococcal disease (IPD)) are available, challenges remain in prevention efforts. Moreover, downstream sequelae in children is relatively unknown. Thus, we aimed to evaluate short and long-term health outcomes among children with IPD. Methods: Analysis of Streptococcus pneumoniae positive isolates from sterile body sites in children (0-17 years) in Alberta (Canada) from 1999 to 2019 was performed retrospectively (n=888). Cases were age and sex-matched to hospitalized population controls. Linkage to administrative health datasets was done to determine comorbidities and healthcare related outcomes. Cox proportional hazards were used to assess differences in time to mortality and hospitalisation between cases and controls in short (<30-day), intermediate (30-90 day), long-term (>90-day) follow-up. Findings: Proportionally more deaths occurred in cases (4.8 deaths/1000 person-years (PY)) than controls (2.7 deaths/1000 PY), leading to a significant adjusted hazard ratio (aHR) of 1.80 (95% CI 1.22-2.64). This increased risk of death was influenced primarily by short-term mortality (319 vs 36 deaths/1000 PY in cases vs controls respectively, aHR 8.78 [95% CI 3.33-23.18]), as no differences were seen in intermediate (14 vs 7 deaths/1000 PY; aHR 2.03, 95% CI 0.41-10.04) or long-term time intervals (2.4 vs 2.3 deaths/1000 PY, aHR 1.03, 95% CI 0.63-1.69). Interpretation: IPD continues to negatively impact survival in children despite vaccination. Although long-term impact on mortality and hospitalisations may not be substantial, the immediate effects of IPD are significant. Funding: This work was supported by grants-in-aid from Pfizer Canada and Wyeth Canada Inc all to GJT.

Tighter precision target required for lactate testing in patients with lactic acidosis.

BACKGROUND: Allowable analytic errors are generally based on biologic variation in normal, healthy subjects. Some analytes like blood lactate have low concentrations in healthy individuals and resultant allowable variation is large when expressed as a coefficient of variation (CV). In Ricós' compendium of biologic variation, the relative pooled intra-individual lactate variation (si) averages 27% and the desirable imprecision becomes 13.5%. We derived biologic variability (sb) from consecutive patient data and demonstrate that sb of lactate is significantly lower. METHODS: A data repository provided lactate results measured over 18 months in the General Systems intensive care unit (ICU) at the University of Alberta Hospital in Edmonton, Canada. In total 54,000 lactate measurements were made on two point-of-care Radiometer 800 blood gas systems operated by Respiratory Therapy. The standard deviations of duplicates (SDD) were tabulated for the intra-patient lactates that were separated by 0-1, 1-2...up to 16 h. The graphs of SDD vs. time interval were approximately linear; the y-intercept provided by the linear regression represents the sum of sb and short-term analytic variation (sa):y0=(sa²+sb²)½. The short-term sa was determined from imprecisions provided by Radiometer and confirmed with onsite controls. The derivation of sb was performed for multiple patient ranges of lactate. RESULTS: The relative desirable lactate imprecision for patients with lactic acidosis is about half that of normal individuals. CONCLUSIONS: As such, evaluations of lactate measurements must use tighter allowable error limits.