Toxic Alcohol Ingestion Research Articles

Falsely elevated osmol gap due to hypertonic hyponatremia

Presence of an elevated osmol gap is frequently used as indirect evidence of toxic alcohol poisoning. We present two cases of suspected toxic alcohol ingestion originating from erroneously calculated osmol gaps secondary to hyperglycemic hyponatremia. Emergency department and poison center staff should be aware of the effect of hyperglycemia on serum sodium, and compensate appropriately when calculating serum osmolarity.

Methanol and ethylene glycol poisoning: a case study and review of current literature

Poisoning is an uncommon but potentially fatal outcome of toxic alcohol ingestion. The toxic alcohols methanol, ethylene glycol and isopropyl alcohol are commonly found in household and commercial products. Because the toxic effects are caused by the metabolites of methanol and ethylene glycol rather than the agents themselves, there is often a substantial delay between ingestion and onset of clinical toxicity. Anion and osmolar gaps are often used for the diagnosis and exclusion of these sometimes subtle overdoses. The pitfalls of using these tests to rule out alcohol ingestion are reviewed. Ethanol infusion is the traditional therapy for such overdoses. In addition to the pathophysiology and clinical findings in poisoning, recent evidence for the use of fomepizole and adjuvant therapies is reviewed.

Increased Osmolal Gap in Alcoholic Acidosis

We studied a patient with alcoholic acidosis and an increased osmolal gap. Ethyl alcohol and other compounds that are known to increase serum osmolality in alcoholics were not detected. However, the levels of glycerol, acetone, and the acetone metabolites acetol and 1,2-propanediol were increased in the serum of this patient. On admission and 3 and 7 hours after admission, the combined serum osmolality of glycerol, acetone, acetol, and 1,2-propanediol accounted for 48%, 92%, and 62% of the increase in the osmolal gap above the highest normal level of 10 mOsm/kg H2O. The disappearance of the osmolal gap correlated with the correction of the acidosis and the concomitant reduction in serum glycerol and acetone levels. Elevations of endogenous glycerol, acetone, and acetone metabolite levels should now be added as causes for an increased osmolal gap in the alcoholic patient. Ingestion of toxic alcohols can no longer be assumed to be the only cause for an increased osmolal gap in alcoholic patients.

Osmol gaps revisited: normal values and limitations.

A study was designed to define the osmol gap in patients whose serum ethanol concentrations are known, to reevaluate several accepted equations for calculating osmolarity, and to apply the results to the theoretical clinical scenario of a toxic alcohol ingestion. The design for the study used consecutive, prospective enrollment of all patients presenting to a large inner city hospital who clinically required determination of their serum ethanol and electrolytes. Three hundred and twenty one consecutive adult patients were enrolled in the study, sixteen were excluded from the final analysis. A stepwise multiple linear regression analysis was performed to determine the best coefficients for sodium, blood urea nitrogen, and ethanol from the data set. Osmolarity was then calculated using these coefficients and traditional models. The osmol gap (measured osmolality minus calculated osmolarity [2*Na + BUN/2.8 + Glu/18 + Etoh/4.6]) was -2 +/- 6 mOsm. Although different equations produced different osmol gaps (ranging from -5 to + 15 mOsm) the standard deviations and correlation coefficients were similar. Large variations exist in the range of osmol gaps. Absolute values are very dependent on the equations used to calculate osmolarity. Because of the larger range of values, small osmol gaps should not be used to eliminate the possibility of toxic alcohol ingestion.

Increased Osmolal Gap in Alcoholic Ketoacidosis and Lactic Acidosis

To determine whether an elevated osmolal gap is specific for toxic alcohol ingestion. Cross-sectional. Emergency room and medical and surgical inpatient wards at a university-affiliated hospital. Twenty-three patients with lactic acidosis, 19 with alcoholic ketoacidosis, and 10 randomly selected controls. Calculated and measured serum osmolality was determined in all study participants. The osmolal gap was increased in patients with lactic acidosis (17.4 +/- 5.4 mmol/kg) and alcoholic ketoacidosis (26.9 +/- 7.6 mmol/kg) when compared with controls (-1.7 +/- 1.7 mmol/kg, P less than 0.05 for both comparisons). When ethanol was included in the calculation, the osmolal gap remained elevated in the lactic acidosis (10.3 +/- 2.0 mmol/kg) and alcoholic ketoacidosis (11.1 +/- 3.2 mmol/kg) groups (P less than 0.05 for both comparisons). The osmolal gap is often used as a screen for toxic alcohol ingestion. When calculating the osmolal gap, the contribution of ethanol should be considered. An elevated osmolal gap is not specific for toxic alcohol ingestion, as the osmolal gap was elevated in patients with lactic acidosis and alcoholic ketoacidosis. These two conditions should be considered when using the osmolal gap to design therapy (for example, hemodialysis) in the setting of anion gap metabolic acidosis and suspected toxic alcohol ingestion.

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Due to the nationwide lockdown to mitigate the spread of COVID-19 and subsequent alcohol ban in South Africa, several cases of toxic alcohol ingestion presented to our emergency unit. Many of these patients admitted to making home brews of alcohol while others simply use industrial toxic alcohols. The diagnosis of these poisonings is challenging as direct assays are not available in our setting.We present a case of presumed ethylene glycol poisoning that presented with persistent seizures and a high anion gap metabolic acidosis (HAGMA).A high index of suspicion for toxic alcohol poisoning should be maintained in patients presenting with an altered mental status, seizures and a HAGMA. Indirect markers such as clinical features and laboratory results can lead to the diagnosis when direct assays are unavailable.

The chemical basis of emergency treatment for the ingestion of toxic alcohols

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe chemical basis of emergency treatment for the ingestion of toxic alcoholsC. H. Breedlove Cite this: J. Chem. Educ. 1982, 59, 12, 1031Publication Date (Print):December 1, 1982Publication History Received3 August 2009Published online1 December 1982Published inissue 1 December 1982https://doi.org/10.1021/ed059p1031RIGHTS & PERMISSIONSArticle Views111Altmetric-Citations-LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (621 KB) Get e-Alerts Get e-Alerts