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. 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. 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. Not applicable
Qafisheh et al. (Thu,) studied this question.