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Home , Ethylene glycol, Toxic alcohol

PUMP THE BRAKES! A Case of Toxic Ingestion Ishan A. Patel, MD; Riana Wurzburger, MD; Ran Ran, MD

Oregon Health & Science University

PMH: Schizophrenia, Polysubstance abuse, prior multiple foreign Introduction body ingestions Ingestions of toxic occur every year which can include glycol, diethylene glycol, Social history: with mother in her backyard, in a tent. ↑Osmolar ADH , and . Gap Vitals: WNL 2-Hydroxyethoxy- Prompt recognition and treatment limits mortality and morbidity, the most serious of which cause irreversible Physical Exam: Alert, answering simple questions. Otherwise, no ALDH organ damage and death. abnormalities detected. 2-Hydroxyethoxy- acetate+H+ - ↑Anion Case Presentation Labs at pH 7.19 | HCO3 12 | AG 28 | Osm Gap 39 Presentation: SCr 1.23 (bl ~0.7) | AST 647 ALT 875 | Lactate 5.4 | CK 4K Gap ADH & 38-year-old man was found by his mother having a ALDH UA negative | UDS (+)MJ, meth | Panel (-) generalized tonic-clonic (GTC) seizure. He was Diglycolate+H+ taken to the local, rural hospital where he was witnessed to have another GTC which was aborted ADH: Labs at pH 7.24 | HCO - 14 | AG 15 | Osm Gap 36 ALDH: Aldehyde Dehydrogenase with IV lorazepam. 3 Transfer: SCr 1.15 | CK 21,000 | ETOH 68 Metabolism of Diethylene Glycol. His history was limited by his mental status but his Metabolic conversion of diethylene glycol to mother later found an empty bottle of brake fluid near + Labs at pH 7.45 | HCO - 26 | AG 9 | Osm Gap 10 diglycolate+H ultimately is responsible for him at the time of his seizure. 3 generation of anion-gap Discharge: SCr 0.7 | CK 12,000 | LFTs down-trending (AGMA).

-Pre-Hospital- -Rural Hospital- -Transfer- -Tertiary Hospital-

- AMS - Consultation - LifeFlight to - Temporary HD - Seizure activity with Oregon OHSU Line Placed Discharge - Establish IV Poison Control - Begin EtOH drip - Hemodialysis x1 to Home access - Medical - NaHCO3, Vit B1, - x1 from ICU - IV Lorazepam stabilization B6

- Dx: Toxic ingestion of diethylene glycol, seizure, AGMA, High - No access to urgent hemodialysis or fomepizole - Electrolyte Osmolar Gap, lactic acidosis, ALI, AKI, rhabdomyolysis - Transfer to higher level of care required abnormalities improving

Discussion Toxic Alcohols Toxic Metabolites Teaching Points

This case illustrates the common clinical and laboratory findings of a severe toxic • Utilize the Oregon Poison Control Center. alcohol ingestion. This includes new-onset seizure, AKI, ALI, lactic acidosis, Fomepizole severe anion-gap metabolic acidosis, and elevated osmolar gap. • Suspect toxic alcohol ingestion in someone who has high AGMA and high osmolar gap. Prompt recognition of diethylene glycol as the cause of the elevated osmolar gap, ADH in consultation with the Poison Control Center, yielded a positive outcome and • Diethylene glycol ingestion is not always identified in a toxic reversal of severe organ damage, as diethylene glycol is not identified routinely alcohol panel. in a toxic alcohol panel. Acetaldehyde EtOH • Treatment Principles include: Third line treatment of (EtOH) by IV can temporize the metabolism of 1) GI Decontamination toxic alcohols by direct, competitive inhibition of the causative metabolic pathway 2) Antidote (ethanol drip, fomepizole) Formation of toxic metabolites can be 3) Sodium Bicarb - if pH < 7.30 responsible for the generation of active, toxic metabolites. blocked by addition of fomepizole, which blocks the ADH enzyme, or by competitive 4) Vitamin cofactors (B1, B6) References inhibition from ethanol (EtOH). 5) Hemodialysis 1. Kraut JA, Mullins ME. Toxic Alcohols. N Engl J Med. 2018;378(3):270-280. 2. Burns, Edward. “Toxic Alcohol Ingestion.” in the Fast Lane • LITFL, 18 May 2016, lifeinthefastlane.com/toxic-alcohol-ingestion/.