The American journal of emergency medicine · 2025
Ethanol and lactate: Is there a direct association?
СтатьяПоддержка исследования: вне правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Audette Megan, Idowu Damilola, Zosel Amy, Farkas Andrew, Corcoran Justin
Аннотация
INTRODUCTION: Ethanol intoxication is frequently encountered in the Emergency Department (ED), often alongside comorbid conditions. Serum lactate, a clinical biomarker for illness severity, is hypothesized to elevate during acute ethanol intoxication due to altered redox states. Providers may defer lactate testing in intoxicated patients due to interpretation uncertainty, though this relationship remains unquantified.
METHODS: We conducted a retrospective study of two cohorts of adult patients who had a serum ethanol measured during an ED encounter, one in a large academic health system from January 1, 2013 to January 30, 2023 and the other in the Veterans Health Administration (VHA) from 2010 to 2019. Patients with diagnoses or medications associated with lactic acidosis were excluded. A de-identified dataset including laboratory results, demographics, and vital signs were obtained. Descriptive statistics and regression analyses were performed.
RESULTS: In the academic center cohort, regression analysis showed poor correlation between ethanol and lactate concentrations (r2 = 0.00110). Subgroup analyses of ethanol concentrations >80 mg/dL and > 200 mg/dL also showed poor correlation (r2 = 0.00570 and 0.00068 respectively). In the VHA cohort, regression analysis similarly revealed no correlation (Pearson's correlation coefficient r = -0.00019 with P = 0.9899).
DISCUSSION: This retrospective analysis found poor correlation between ethanol and lactate concentrations in both cohorts. Elevated lactate should not be attributed to ethanol alone. While effort was taken to exclude potential confounders, the causes of lactic acidosis are numerous, and confounders may remain. Prospective studies could better clarify any relationship between ethanol and lactate concentrations.
CONCLUSION: Ethanol intoxication does not justify deferring lactate testing when clinically indicated. Elevated lactate concentrations should prompt evaluation for alternative causes.
METHODS: We conducted a retrospective study of two cohorts of adult patients who had a serum ethanol measured during an ED encounter, one in a large academic health system from January 1, 2013 to January 30, 2023 and the other in the Veterans Health Administration (VHA) from 2010 to 2019. Patients with diagnoses or medications associated with lactic acidosis were excluded. A de-identified dataset including laboratory results, demographics, and vital signs were obtained. Descriptive statistics and regression analyses were performed.
RESULTS: In the academic center cohort, regression analysis showed poor correlation between ethanol and lactate concentrations (r2 = 0.00110). Subgroup analyses of ethanol concentrations >80 mg/dL and > 200 mg/dL also showed poor correlation (r2 = 0.00570 and 0.00068 respectively). In the VHA cohort, regression analysis similarly revealed no correlation (Pearson's correlation coefficient r = -0.00019 with P = 0.9899).
DISCUSSION: This retrospective analysis found poor correlation between ethanol and lactate concentrations in both cohorts. Elevated lactate should not be attributed to ethanol alone. While effort was taken to exclude potential confounders, the causes of lactic acidosis are numerous, and confounders may remain. Prospective studies could better clarify any relationship between ethanol and lactate concentrations.
CONCLUSION: Ethanol intoxication does not justify deferring lactate testing when clinically indicated. Elevated lactate concentrations should prompt evaluation for alternative causes.