A 27-year-old man with a history of depression presents after a reported ingestion of “about 8 ounces” of a workplace industrial solvent that has been identified by a shift supervisor as diethylene glycol. You are familiar with ethylene glycol and wonder if diethylene glycol poisoning results in similar toxicity. The patient has normal vital signs and a normal examination. What laboratory testing is warranted in this patient? Is it possible to obtain a diethylene glycol level? Based on this reported ingestion, what treatment is warranted?
A 54-year-old man you admitted on your last shift for severe alcohol withdrawal remains on a lorazepam infusion that you started 24 hours ago in the ED. When following up his case, you note that the patient has developed a worsening lactic acidosis since his admission. You discuss the case with the intensivist who is caring for the patient in the ICU. His infectious workup has been normal, and the rest of his laboratory testing has been within normal limits. What is the etiology of his lactic acidosis?
A 67-year-old man with a history of alcohol abuse is brought in by EMS after he was found unconscious outside a grocery store. EMS notes that the patient is responding to painful stimuli only and had an episode of blood-tinged emesis on the scene. He arrives to the ED receiving oxygen via nonrebreather mask. An empty bottle of rubbing alcohol is found in his coat pocket. What are your concerns in a patient with likely isopropanol exposure? What laboratory workup is warranted?
The term toxic alcohol refers to a group of hydrocarbons that contain a hydroxyl group (-OH group) and are not intended for ingestion. This group includes ethylene glycol, methanol, propylene glycol, and isopropanol.1 Diethylene glycol belongs to a class of glycol ethers that contain hydroxyl groups. It is also discussed here, as it may present in a clinically similar fashion to the toxic alcohols.2
Ethylene glycol is used primarily as an engine coolant, antifreeze, or brake fluid, and it may be unintentionally consumed by children or animals because of its sweet taste.1,3 Methanol, most commonly in the form of windshield-washer fluid, has been implicated in several poisoning epidemics resulting from tainted beverages.1,4-7 Outbreaks have been reported in undeveloped countries as a result of the adulteration of ethanol with methanol. Diethylene glycol, used as an antifreeze and as a solvent in industry and manufacturing, is responsible for multiple mass poisoning events due to its unsafe use as a diluent in medications and as a sweetener in wines, and it has also been used in self-harm attempts.2,8-14 In 1937, 107 deaths followed ingestion of diethylene glycol that was used as a diluent for an elixir of the antibiotic sulfanilamide. This incident led to passage of the 1938 Food, Drug, and Cosmetic Act, which made the declaration that pharmaceutical products must be shown to be safe prior to public marketing.15 Propylene glycol, present in many foods, beverages, and cosmetics, is used as a diluent in many pharmaceuticals and also as an alternative to ethylene glycol in some antifreeze products.16 Isopropanol, or isopropyl alcohol, is typically available as a 70% rubbing alcohol solution and may be abused as an ethanol substitute. It is also a solvent used in household and pharmaceutical products.1
All of the toxic alcohols may cause altered mental status, due to both increased inhibitory gamma-aminobutyric acid (GABA) tone and inhibition of the excitatory N-Methyl-D-aspartic acid (NMDA) glutamate receptors.1 The metabolism of toxic alcohols to their metabolites may result in acidosis or ketosis. Specific end-organ toxicity from toxic alcohol metabolites is possible, including glycolic acid in ethylene glycol exposure, formic acid in methanol exposure, (2-hydroxyethoxy)acetic acid (HEAA) in diethylene glycol exposure, lactate in propylene glycol exposure, and acetone in isopropanol exposure.1,2
The presence of a metabolic acidosis should also prompt consideration of other causes, including poisoning by xenobiotics such as metformin, which can cause a lactic acidosis; cellular poisoning by salicylate, iron, or cyanide; diabetic, alcoholic, or starvation ketosis; renal failure; and multiorgan failure from critical systemic illness such as sepsis.
A large difference in measured osmolarity and calculated osmolality (the osmol gap) should prompt consideration of a toxic alcohol exposure; however, this finding is neither sensitive nor specific and cannot be used to definitively rule in or rule out this exposure.
Disposition of the critically ill patient with toxic alcohol exposure requires consideration of patient needs, including access to antidotal therapies (such as fomepizole or ethanol), the availability of hemodialysis services, if needed, and an inpatient unit capable of providing critical care and resuscitation.
To identify primary relevant literature, standard search strategies were used, including querying MEDLINE® with the search terms toxic alcohol, ethylene glycol, methanol, diethylene glycol, propylene glycol, isopropyl alcohol, isopropanol, and fomepizole. Results were reviewed for clinical and practical relevance. Clinical studies, animal studies, review articles, editorials, commentaries, case reports, and case series were identified for review. The Cochrane Database of Systematic Reviews and the National Guideline Clearinghouse (www.guideline.gov) were also queried. Additional information was obtained from book chapters and Internet material.
Evidence-based medicine requires a critical ap¬praisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study are included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the authors, are noted by an asterisk (*) next to the number of the reference.
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Gillian A. Beauchamp, MD; Matthew Valento, MD
September 1, 2016
October 1, 2019
4 AMA PRA Category 1 Credits™, 4 ACEP Category I Credits, 4 AAFP Prescribed Credits, 4 AOA Category 2-A or 2-B Credits. Specialty CME Credits: Included as part of the 4 credits, this CME activity is eligible for 0.5 Pharmacology CME credits
Upon completion of this article, you should be able to:
Date of Original Release: September 1, 2016. Date of most recent review: August 10, 2016. Termination date: September 1, 2019.
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