Abstract Introduction Toxic alcohols (methanol, ethylene glycol, and isopropyl alcohol (IPA)) are important causes of altered mental status (AMS). IPA, ubiquitous in rubbing alcohols and hand sanitizers, is the most frequently reported toxic-alcohol exposure to U.S. poison centers and typically has lower mortality because toxicity reflects CNS depression rather than acidemia. Although ingestion predominates, inhalational and dermal exposures can produce clinically significant systemic levels by bypassing first-pass metabolism. Most exposures are unintentional, though intentional use as an ethanol substitute or in suicide attempts occur. Case Presentation A 79-year-old man with end-stage kidney disease on maintenance hemodialysis, hypertension, type 2 diabetes, compensated HFrEF, and chronic respiratory failure on 2 L/min oxygen was brought to the ED by police for impaired driving after a negative roadside ethanol test. He was alert but disoriented (GCS 11); vitals were stable. Examination showed gait instability without focal deficits. Labs were unremarkable except BUN 83 mg/dL. He underwent hemodialysis with 2 L ultrafiltration and continued home medications, with transient improvement. The next day his encephalopathy worsened (GCS 9-10), prompting ICU admission for close neurologic and airway monitoring. A broad evaluation including CT head; ammonia, TSH, B12, and folate; and an ABG without hypercapnia was unrevealing. Repeat BUN decreased to 35-40 mg/dL (baseline). Collateral history revealed habitual sniffing of rubbingalcohol; nursing staff also reported repeated requests for alcohol swabs provided with good intentions. With strict avoidance of isopropyl products, his mental status and gait progressively improved. He was discharged in stable condition with exposure-avoidance counseling and follow-up with nephrology and primary care. Discussion AMS with an alcohol odor but a negative ethanol level should prompt consideration of IPA. Non-oral routes are easily missed; targeted questions about product type and inhalational/dermal exposure are essential. With ingestion, hemorrhagic gastritis is common, whereas non-oral exposures may lack GI symptoms and delay recognition. IPA is oxidized by hepatic alcohol dehydrogenase to acetone, a neutral ketone and milder CNS depressant; therefore, ADH inhibition (fomepizole) is not indicated in isolated IPA poisoning. When ethanol is negative, obtain a blood volatile panel by headspace gas chromatography to identify isopropanol and acetone. The characteristic pattern is ketosis without an anion-gap metabolic acidosis, often with an early osmolal gap; acetone can falsely elevate creatinine via Jaffe assay interference (“pseudo-renal failure”). Management is primarily supportive (airway protection, IV fluids, GI protection). Hemodialysis is reserved for severe illness or very high IPA concentrations (≥500 mg/dL). This abstract is funded by: None
Sayed et al. (Fri,) studied this question.