Abstract

Presence of ethanol (EtOH) may alter the relationship between clinically measured lactate concentrations and mortality. This study will assess how the prognostic value of serum lactate concentrations changes based on the presence of EtOH. We performed a retrospective cohort study including all patients, age > 17 years, presenting from January 2012 through December 2018, to an urban, academic emergency department (ED). Patients without ED lactate measurements were excluded. Data were electronically abstracted from the medical record, including demographics, initial lactate level, blood and urine EtOH levels, administration of antibiotics, inclusion in trauma registry, vasopressor administration and 28-day in-hospital mortality. We manually abstracted data from 1000 randomly selected cohort patients to test reliability of the automated abstraction process. The primary outcome was 28-day in-hospital mortality. Initial ED lactate levels were re-grouped using 1.0 mmol/L unit intervals: 0.0-0.9, 1.0-1.9, 2.0-2.9, 3.0-3.9, 4.0-4.9, 5.0-5.9, 6.0-6.9, 7.0-7.9, and >8.0 mmol/L. EtOH levels were grouped as Present (any EtOH present), Absent (EtOH level measured and not detected), and Missing (not ordered). Available urine EtOH levels were utilized if blood EtOH was absent. Using logistic regression and a priori selected mortality risk factors, we created a baseline model to predict 28-day in-hospital mortality for the entire cohort. Among patients with ED lactate measured, we calculated marginal probabilities for mortality, beyond the baseline model, for each lactate interval, using 95% confidence intervals to assess differences. Over seven years, 441,613 adult patient encounters occurred, and 40,956 (9.27%) patients had lactate measured: 4,219 (10.30%) EtOH Present, 11,181 (27.30%) Absent, and 25,556 (62.40%) Missing patients. Overall, 2374 (5.8%, 95% CI 5.6-6.0%) had 28-day in-hospital mortality and this varied by EtOH group: 201 (4.8%, 4.1-5.5%) Present, 916 (8.2%, 7.7-8.7%) Absent, and 1257 (4.9%, 4.7-5.2%) Missing patients. In EtOH Present patients, 3511 (83.2%, 82.1-84.3%) had initial lactate >2.0 mmol/L compared to 4975 (44.5%, 43.6-45.4%) of Absent patients. In logistic regression, after controlling for other predictors of mortality, lactate intervals predicted a higher marginal probability of mortality in the EtOH Absent group compared with Present, until lactate exceeded 6.0 mmol/L: 1.0-1.9 (1.77% (95% CI: 1.42-2.12%) vs 0.27% (0-0.54%)); 2.0-2.9 (2.42% (1.89-2.96%) vs 0.43% (0.16-0.70%)); 3.0-3.9 (1.72% (1.19-2.26%) vs 0.67% (0.29-1.05%)); 4.0-4.9 (2.95% (2.00-3.91%) vs 1.08% (0.41-1.75%)); 5.0-5.9 (3.12% (1.89-4.36%) vs 1.02% (0.30-1.74%)); 6.0-6.9 (3.41% (1.79-5.03%) vs 1.51% (0.32-2.70%)). EtOH may diminish the relationship between initial lactate levels and 28-day in-hospital mortality, decreasing lactate’s prognostic utility in the ED. Clinicians using lactate to risk stratify patients should use caution in the presence of EtOH.

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