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Objective: To study the effect of stress hyperlactatemia on the association between stress hyperglycemia and mortality. Design: Retrospective cross-sectional observation study. Setting: Three ICUs using arterial blood gases with simultaneous glucose and lactate measurements during ICU stay. Patients: Cohort ot 7,925 consecutive critically ill patients. Interventions: None. Measurements and Main Results: We analyzed 152,349 simultaneous measurements ot glucose and lactate. We performed multivariabie analysis to study the association ot different metrics of glucose and lactate with hospital mortality. On day 1, first (p = 0.013), highest (p = 0.001), mean (p = 0.019), and time-weighted mean (p = 0.010) glucose levels were associated with increased mortality. A similar, but stronger, association was seen tor corresponding lactate metrics (p < 0.0001 tor all). However, once glucose and lactate metrics were entered into the multivariable logistic regression model simultaneously, all measures of glycemia ceased to be significantly associated with hospital mortality regardless of the metrics being used (first, highest, mean, timeweighed; p > 0.05 for all), whereas all lactate metrics remained associated with mortality (p < 0.0001 for all). In patients with at least one episode of moderate hypoglycemia (glucose ⩽ 3.9 mmol/L), glucose metrics were not associated with mortality when studied separately (p > 0.05 for all), whereas lactate was (p < 0.05 for all), but when incorporated into a model simultaneously, highest glucose on day 1 was associated with mortality (p < 0.05), but not other glucose metrics (p > 0.05), whereas all lactate metrics remained associated with mortality (p < 0.05 for all). Conclusions: Stress hyperlactatemia modifies the relationship between hyperglycemia and mortality. There is no independent association between hyperglycemia and mortality once lactate levels are considered. [ABSTRACT FROM AUTHOR]

Objective: Acute kidney injury in the critically ill is an independent risk factor for adverse outcome. The magnitude of the impact of acute kidney injury on outcome, however, is still unclear. This study aimed to estimate the excess mortality attributable to acute kidney injury. Design: We performed a sequentially matched analysis according to the day of acute kidney injury diagnosis after ICU admission. Patients with acute kidney injury and those without acute kidney injury were matched according to age, sex, ICU admission diagnosis, Simplified Acute Physiology Score II without renal and age components, and the propensity to develop acute kidney injury at each of the four matching time points. Setting: Cohort of 16 participating ICUs from the prospective Finnish Acute Kidney Injury study. Patients: Cohort of 2,719 consecutive patients with either emergency admission or elective postsurgical patients with an expected ICU stay greater than 24 hours. Interventions: None. Measurements and Main Results: Of the 2,719 patients included in the study, acute kidney injury developed in 1,081 patients (39.8%) according to the Kidney Disease: Improving Global Outcomes-definition during ICU treatment on days 1-5. Of these, 477 patients were successfully matched to 477 patients who did not develop acute kidney injury. The 90-day mortality of the matched patients with acute kidney injury was 125 of 477 (26.2 %) compared with 84 of 477 (17.6%) for their matched controls without acute kidney injury. Thus, the absolute excess 90-day mortality attributable to acute kidney injury was estimated at 8.6 percentage points (95% Cl, 2.6-17.6 percentage points). The population attributable risk (95% Cl) of 90-day mortality associated with acute kidney injury was 19.6% (10.3-34.1 %). Conclusions: In general ICU patients, the absolute excess 90-day mortality statistically attributable to acute kidney injury is substantial (8.6%), and the population attributable risk was nearly 20%. Our findings are useful in planning suitably powered future clinical trials to prevent and treat acute kidney injury in critically ill patients. [ABSTRACT FROM AUTHOR]