No ingestion, no inhalation, still toxic: Acetone poisoning via skin absorption

Authors

• Qutaiba Qafisheh, Department of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
• Roaa Aljunaidi, Faculty of Medicine and Health Sciences, Palestine Polytechnic University, Hebron, Palestine. Roaa.aljunaidi2@gmail.com.
• Abdalhakim Shubietah, Advocate Health - MidwestFollow
• Muath A. Baniowda, Department of Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA.
• Mohamed S. Elgendy, Faculty of Medicine, Tanta University, Tanta, Egypt.
• Ahmed Emara, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
• Mohanad Qwaider, Department of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
• Nezam Altorok, Division of Rheumatology and Immunology, Department of Internal Medicine, The University of Toledo Medical Center, Toledo, OH, USA.

Recommended Citation

Qafisheh Q, Aljunaidi R, Shubietah A, et al. No ingestion, no inhalation, still toxic: acetone poisoning via skin absorption. Int J Emerg Med. 2026;19(1):199. Published 2026 Aug 6. doi:10.1186/s12245-026-01286-y

Affiliations

Advocate Illinois Masonic Medical Center

Abstract

Background: Acetone toxicity is typically associated with ingestion or inhalation, whereas clinically meaningful transdermal absorption is uncommon and may be overlooked, particularly in patients with impaired skin barriers.

Case presentation: A 48-year-old man with C4 quadriplegia, a chronic sacral ulcer, and cranial cortical stimulation electrodes from the ReHAB trial presented with two weeks of poor oral intake and progressive encephalopathy culminating in respiratory failure. Initial testing showed high anion-gap metabolic acidosis with an elevated osmolar gap (pH 7.22; HCO₃ 6 mmol/L; anion gap 28 mmol/L; measured osmolality 453 mOsm/kg), beta-hydroxybutyrate 7.2 mmol/L, and serum acetone 29.8 mg/dL, with undetectable isopropanol and other toxic alcohols. Additional history revealed topical isopropyl alcohol application to scalp connector sites approximately 36 h before presentation. The patient improved with intravenous fluids and bicarbonate therapy, required brief mechanical ventilation, and returned to baseline mentation by hospital day 9.

Conclusion: This case demonstrates two concurrent mechanisms: starvation ketoacidosis as the primary driver of anion-gap acidosis and transdermal isopropyl alcohol exposure with hepatic conversion to acetone as a plausible contributor to acetonemia and the elevated osmolar gap. Clinicians should consider noningestional exposures in unexplained dual-gap acidosis, especially in patients with neurodisability and device-adjacent or compromised skin.

Clinical trial number: Not applicable.

Type

Article

PubMed ID

42563149