4.3 Article

Distinguishing between toxic alcohol ingestion vs alcoholic ketoacidosis: how can we tell the difference?

Journal

CLINICAL TOXICOLOGY
Volume 59, Issue 8, Pages 715-720

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/15563650.2020.1865542

Keywords

Ethanol; alcoholic ketoacidosis; methanol; ethylene glycol; toxic alcohol; anion gap metabolic acidosis

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This study aimed to retrospectively analyze data from a US Poison Control Center over nearly 20 years to explore diagnostic differences and related factors between alcoholic ketoacidosis (AKA) and toxic alcohol ingestion. The results showed that as ethanol concentration increased, the odds of diagnosing AKA also increased.
Context: Anion gap metabolic acidosis (AGMA) is common in patients presenting for emergency care. While some disease processes and ingestions are easily excluded, diagnosing toxic alcohol (TA) ingestion can be challenging. This is especially true if drug concentrations are not readily available, which forces clinicians to rely on surrogate markers. Like TA ingestion, alcoholic ketoacidosis (AKA) produces an elevated osmol gap and an AGMA. The aim of this study was to identify risk factors suggestive of AKA when TA ingestion was the primary alternative differential diagnosis. We hypothesized that the odds of an AKA diagnosis would increase as ethanol concentration increased. Methods: This was a retrospective analysis of data from 2000 through 2019 from a single US Poison Control Center. Records were reviewed to identify cases coded as methanol or ethylene glycol; or coded as alcohol or ethanol with acidosis. The case definition for AKA required: (1) documented alcohol use disorder; (2) urine or serum ketones or elevated blood beta-hydroxybutyrate concentration; (3) anion gap >= 14 mmol/L. The inclusion criterion for TAs was a detectable methanol or ethylene glycol concentration. Results: Of 699 patients screened, 86 were diagnosed with AKA and 36 were diagnosed with TA ingestion. As ethanol concentration increased, the odds of an AKA diagnosis significantly increased (OR = 1.016, 95% CI 1.002-1.031, p = .03). Conclusions: In this retrospective analysis, the odds of diagnosing AKA instead of TA ingestion increased as ethanol concentration increased. The limited ability of common clinical factors to differentiate these diagnoses highlights the need to obtain quantitative TA concentrations in real time. Until prospective validation, interpretation of ketone concentrations and toxic alcohol concentrations (when available) will continue to guide decision making.

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