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Emergency and Acute Medicine – Isopropanol poisoning
Isopropanol is a central nervous system depressant that is two to three times more potent than ethanol. It is rapidly absorbed after ingestion and is metabolized by alcohol dehydrogenase to acetone, which is also a CNS depressant. Unlike other toxic alcohols, isopropanol is ketogenic but does not cause a significant metabolic acidosis. Acetone is eliminated by the lungs and kidneys. The half-life of isopropanol ranges from 3 to 16 hours, while acetone has a longer half-life of 7.5 to 26 hours. Concomitant ethanol ingestion prolongs the half-life of isopropanol but not acetone.
Isopropanol is a clear, colorless, volatile liquid with a faint acetone odor and bitter taste, commonly found as 70% rubbing alcohol. It is present in many household and industrial products including disinfectants, hand sanitizers, solvents, window cleaners, paint removers, detergents, antifreeze, and toiletries. The typical adult patient is a chronic alcoholic who ingests isopropanol after depleting ethanol supplies. Dermal, inhalational, and rectal exposures can also cause systemic toxicity. Accidental ingestions are common in young children.
Symptoms usually develop within 30 to 60 minutes of exposure. Neurologic manifestations include lethargy, inebriation, vertigo, ataxia, headache, weakness, respiratory depression, coma, and apnea, without the initial excitatory phase seen with ethanol. Gastrointestinal findings include nausea, vomiting, abdominal pain, gastritis, and hematemesis. Cardiovascular effects include hypotension, tachycardia, myocardial depression, and peripheral vasodilation. Pulmonary findings include respiratory depression and hemorrhagic tracheobronchitis. Skin and eye exposure may cause irritation or chemical burns.
Diagnosis is based on history of exposure and the characteristic odor of isopropanol or acetone on the breath. Laboratory evaluation typically shows ketosis without significant acidosis unless end-organ hypoperfusion is present. Hypoglycemia may occur, particularly in children. Acetone can falsely elevate serum creatinine, which normalizes as acetone is metabolized. Urinalysis shows ketones, and an elevated osmolar gap is common. Coma is associated with serum isopropanol levels greater than 150 mg/dL. Imaging is guided by clinical findings, with chest radiography used to assess for aspiration and head CT considered for possible trauma.
Management is primarily supportive, with attention to airway protection, breathing, and circulation. Hypotension is treated with intravenous fluids and vasopressors if needed. There is no specific antidote, and treatment with ethanol or fomepizole is contraindicated. Activated charcoal may be considered if coingestants are suspected. Skin and eye exposures require copious irrigation. Hemodialysis effectively removes isopropanol and acetone and is reserved for patients with refractory hypotension, severe toxicity, or serum levels greater than 400 mg/dL.
Patients with moderate to severe toxicity, including altered mental status or hypotension, require hospital admission. Asymptomatic or mildly intoxicated patients may be observed for 2 to 4 hours and discharged if symptoms resolve. Referral for alcohol detoxification or psychiatric evaluation is recommended for intentional ingestions.
Supportive care remains the cornerstone of treatment, and a key pitfall is inappropriate use of ethanol or fomepizole, which should be avoided in isopropanol poisoning.
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