Isopropyl Alcohol

How to Cite This Chapter: Perri D, Klimaszyk D, Kołaciński Z, Szajewski J. Isopropyl Alcohol. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.20.2.4.?utm_source=nieznany&utm_medium=referral&utm_campaign=social-chapter-link Accessed December 12, 2024.
Last Updated: February 17, 2022
Last Reviewed: February 17, 2022
Chapter Information

Unit conversion table: see Table 1 in Alcohols.

Isopropyl alcohol (isopropanol) is a solvent, antiseptic, and disinfectant often found in the home as a 70% solution (rubbing alcohol). It is sometimes used by alcohol abusers as a cheap substitute for ethanol. Unlike methanol and propylene glycol, isopropyl alcohol is not metabolized to toxic organic acids. It is well absorbed within 90 to 120 minutes and quickly distributes into body water. It is metabolized by alcohol dehydrogenase to acetone. Although rare and usually reported in children, toxicity may result from skin and inhalational exposure.

Mechanism of toxicity: Isopropyl alcohol is 2 to 3 times more potent a central nervous system (CNS) depressant than ethanol. Its metabolism to acetone (another CNS depressant) can prolong sedation or coma. Large ingestions may lead to respiratory arrest, hypotension due to vasodilation, and myocardial suppression. It is very irritating to the gastrointestinal mucosa and gastritis is common.

Toxic dose: Toxic ingestions have occurred at oral doses of 0.5 to 1 mL/kg of 70% isopropyl alcohol solution. Fatal ingestions have been reported with volumes of 200 to 250 mL, but this depends on individual tolerance and coingestions.

Clinical FeaturesTop

1. Isopropyl alcohol intoxication begins similar to ethanol intoxication with confusion, slurred speech, and postural instability, but with greater exposure (serum levels >25 mmol/L [150 mg/dL]) it can ultimately lead to coma, respiratory arrest, and hemodynamic instability. Acetone can contribute to CNS depression.

2. Gastric symptoms including pain and vomiting are more prevalent than with other alcohols, and severe gastritis may present with hematemesis.

DiagnosisTop

The clinical diagnosis of isopropyl alcohol toxicity should be suspected with a history of ingestion, elevated osmolar gap, absence of a significant anion gap, and typical smell of isopropanol or acetone.

Diagnostic Tests

1. Specific testing for the isopropyl alcohol serum level is available from most toxicology laboratories. Acetone can be detected in blood within 1 hour and in urine within 3 hours of ingestion of isopropyl alcohol. When not available, the serum level may be estimated from the osmolar gap (formulas: see Alcohols).

2. Other suggested investigations include electrolyte levels, blood glucose levels, blood urea nitrogen, osmolality (to calculate anion and osmolar gaps), as well as arterial blood gases. Ketones may be detected in blood and urine within 3 hours from ingestion. Oximetry and chest radiographs may be helpful for patients with a decreased level of consciousness or suspected aspiration.

TreatmentTop

1. Decontamination: Since isopropyl alcohol is rapidly absorbed, gastric emptying procedures (like aspiration of stomach contents) are unlikely to offer benefit unless patients with large ingestions present within 20 to 30 minutes of ingestion.

2. Antidotes and specific therapies: There is no antidote. Ethanol and fomepizole are not necessary, as there are no toxic organic acids formed from isopropyl alcohol metabolism.

3. Accelerated elimination: Hemodialysis can remove isopropyl alcohol and acetone but most patients are successfully treated with supportive care alone. Dialysis is rarely necessary and reserved for massive ingestions (isopropyl levels >80 mmol/L [500 mg/dL]), in the presence of acute kidney injury, and if hypotension does not respond to fluid resuscitation and vasoactive medication.

4. Supportive care:

1) Ensure airway patency and intubate and assist ventilation if necessary.

2) Watch for and treat coma and hypotension.

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