Isopropanol (isopropyl alcohol) is the most commonly ingested toxic alcohol, found in rubbing alcohol, hand sanitizers, and household cleaners. It is metabolized by alcohol dehydrogenase to acetone (not to an organic acid), producing the hallmark finding of ketonemia/ketonuria without metabolic acidosis — a key distinguishing feature from methanol and ethylene glycol poisoning. [1-2] Although it frequently causes medical complications, deaths are rare with prompt supportive care. [1-2]
The following algorithm from the NEJM review on toxic alcohols outlines the diagnostic and management approach:
1. History
- Substance ingested: rubbing alcohol (70% isopropanol), hand sanitizer, cleaning products, solvents, antifreezes, cosmetics [2]
- Amount and concentration ingested; as little as 1 mL/kg of 70% solution can produce symptoms
- Time of ingestion — rapid absorption with peak plasma levels within 30 minutes [2]
- Route: oral (most common), inhalation, or dermal exposure [2]
- Intentional (suicidal, inebriation substitute) vs. accidental (most common in children <6 years) [2]
- Coingestion: ethanol, other toxic alcohols, medications (especially sedatives)
- Symptoms: nausea, vomiting, abdominal pain, dizziness, headache, slurred speech
- Progression: inebriation → CNS depression → obtundation → coma
2. Alarm Features
- Deep coma — serum isopropanol >150 mg/dL (25 mmol/L) [1]
- Cardiovascular collapse / refractory hypotension [1-2]
- Respiratory depression requiring intubation
- Lactic acidosis — suggests severe tissue hypoperfusion [1]
- Hemorrhagic gastritis with GI bleeding
- Acute pancreatitis [1]
- Serum isopropanol ≥500 mg/dL — threshold for hemodialysis consideration [1]
3. Medications
- Do NOT use fomepizole or ethanol — alcohol dehydrogenase inhibitors slow the removal of isopropanol and should not be used (this is the opposite of methanol/ethylene glycol management) [1]
- IV fluids — isotonic crystalloid for hypotension
- Vasopressors if refractory hypotension
- Antiemetics for nausea/vomiting
- Avoid sedatives/opioids that compound CNS depression
- No role for activated charcoal (isopropanol is rapidly absorbed and poorly adsorbed by charcoal)
4. Diet
- NPO if altered mental status or risk of aspiration
- Hydration is critical — IV fluids to support renal elimination
- No specific dietary triggers; this section is less applicable to acute toxicology
5. Review of Systems
- Neuro: level of consciousness, headache, dizziness, ataxia, visual changes (to distinguish from methanol)
- GI: nausea, vomiting, hematemesis, abdominal pain (epigastric — consider hemorrhagic gastritis or pancreatitis)
- Respiratory: dyspnea, respiratory rate/effort
- Cardiovascular: lightheadedness, syncope, chest pain
- Renal: urine output
- Psych: suicidal ideation, intent, plan (if intentional ingestion)
6. Collateral History and Family History
- Witnesses to ingestion — what product, how much, when
- Access to other substances (coingestants)
- Psychiatric history, prior suicide attempts, substance use disorder
- Family history is generally not contributory in acute toxicology
- Social context: homelessness, alcohol use disorder (isopropanol used as ethanol substitute), occupational exposure
7. Risk Factors
- Alcohol use disorder — isopropanol used as ethanol substitute
- Psychiatric illness / suicidal ideation
- Pediatric age (<6 years) — most exposures are unintentional [2]
- Occupational exposure (cleaning, industrial settings)
- Homelessness
- Access to concentrated products (99% isopropanol, e.g., ISO-HEET®) [3]
8. Differential Diagnosis
- Ethanol intoxication — no ketosis, positive ethanol level, no osmol gap from other sources
- Methanol poisoning — high anion-gap metabolic acidosis (HAGMA), visual changes, formate elevation; onset 6–24 hours [1]
- Ethylene glycol poisoning — HAGMA, calcium oxalate crystalluria, AKI, hypocalcemia; onset 12–24 hours [1]
- Diabetic ketoacidosis — hyperglycemia, elevated β-hydroxybutyrate, HAGMA
- Alcoholic ketoacidosis — history of chronic ethanol use, HAGMA, elevated β-hydroxybutyrate (isopropanol has low/absent β-hydroxybutyrate) [4]
- Starvation ketosis
- Other sedative-hypnotic overdose (benzodiazepines, barbiturates, GHB)
Key distinguishing feature: Isopropanol produces elevated osmol gap + ketonemia/ketonuria WITHOUT anion-gap metabolic acidosis, unlike methanol and ethylene glycol which produce HAGMA. β-hydroxybutyrate is undetected or low in isopropanol poisoning, helping distinguish it from DKA and AKA. [2][4-5]
9. Past Medical History
- Prior toxic ingestions or suicide attempts
- Alcohol use disorder or substance use history
- Chronic liver disease (impaired metabolism)
- Chronic kidney disease (impaired elimination)
- Psychiatric diagnoses
- Chronic pancreatitis (increased risk of acute pancreatitis)
10. Physical Exam
- Vitals: Hypotension, tachycardia, tachypnea (if compensating for acidosis from secondary causes), hypothermia
- General: Fruity/sweet (acetone) odor on breath [2][6]
- Neuro: Depressed sensorium ranging from lethargy to deep coma; ataxia, slurred speech, nystagmus; absent focal neurologic deficits
- HEENT: Pupils — typically normal (mydriasis possible); no visual field deficits (distinguishes from methanol)
- Abdomen: Epigastric tenderness (hemorrhagic gastritis, pancreatitis)
- Respiratory: Assess for respiratory depression, aspiration
- Skin: Assess for dermal exposure; check for signs of IV drug use or other trauma
11. Lab Studies
- BMP: Normal anion gap is the hallmark; check glucose, electrolytes, BUN/Cr (note: acetone can spuriously elevate creatinine via Jaffe reaction interference) [1]
- Serum osmolality (by freezing-point depression) and calculated osmolality → elevated osmol gap [2][6]
- Calculated osmolality = 2(Na) + glucose/18 + BUN/2.8
- Osmol gap >10 mOsm/kg is significant
- Serum isopropanol and acetone levels (if available via gas chromatography) [2]
- 50 mg/dL = clinically significant
- 150 mg/dL = deep coma
- ≥500 mg/dL = consider hemodialysis [1]
- Urinalysis: Ketonuria (positive nitroprusside reaction from acetone) WITHOUT glycosuria [1-2]
- Serum β-hydroxybutyrate: Low or absent (helps distinguish from DKA/AKA) [4]
- Lactate: Elevated lactate suggests severe poisoning with tissue hypoperfusion [1]
- Serum ethanol level: Rule out coingestion (ethanol delays isopropanol metabolism)
- Lipase: If abdominal pain (acute pancreatitis) [1]
- CBC: Assess for anemia if GI bleeding suspected
- VBG/ABG: Confirm absence of metabolic acidosis (key differentiator)
- Acetaminophen, salicylate levels: Standard in intentional ingestion workup
12. Imaging
- Chest X-ray: If respiratory depression, aspiration risk, or intubated
- CT head: If altered mental status is disproportionate to expected toxicity or if trauma suspected
- Imaging is generally not required for straightforward isopropanol ingestion
- Abdominal imaging only if concern for surgical pathology
13. Special Tests
- Osmol gap calculation — the most useful bedside diagnostic tool [6]
- Gas chromatography / HPLC — definitive identification and quantification of isopropanol and acetone, but often not rapidly available [1]
- Point-of-care glucose — rule out hypoglycemia in altered mental status [7]
- Poison Control consultation (800-222-1222) — recommended for all toxic alcohol exposures [7]
14. ECG
- Obtain ECG in all intentional ingestions to rule out coingestant effects
- Isopropanol itself does not produce characteristic ECG changes
- Monitor for sinus tachycardia (most common finding)
- Assess for QTc prolongation, conduction delays, or dysrhythmias suggesting coingestant (e.g., tricyclic antidepressants) [6]
15. Assessment
Isopropanol is approximately twice as intoxicating as ethanol but has a lower mortality than methanol or ethylene glycol because its metabolite (acetone) is a ketone, not an organic acid. [1-2] The classic metabolic signature is:
- ↑ Osmol gap
- Ketonemia/ketonuria (acetone)
- Normal anion gap / no metabolic acidosis (unless secondary lactic acidosis from cardiovascular collapse)
- Normal bicarbonate
Clinical effects onset within 2–4 hours of ingestion. [1] Isopropanol half-life is 2.5–8 hours; acetone half-life is 7.7–27 hours (acetone may cause prolonged CNS depression). [2] Most patients make a full recovery with supportive care. [2]
Complications: Hemorrhagic gastritis, acute pancreatitis, rhabdomyolysis, aspiration pneumonia, cardiovascular collapse. [1-2]
16. Treatment Plan
Initial stabilization
- ABCs — intubate if GCS ≤8 or loss of airway protective reflexes
- IV access, continuous cardiac monitoring, pulse oximetry
- IV crystalloid bolus for hypotension; vasopressors if refractory
Decontamination
- Activated charcoal is NOT recommended (rapid absorption, poor adsorption)
- Gastric lavage is generally not indicated unless massive ingestion within 30–60 minutes
Supportive care (mainstay of treatment)
- IV fluids to maintain euvolemia and support renal elimination
- Antiemetics PRN
- Monitor and treat hypoglycemia
- Serial neurologic assessments
Hemodialysis indications: [1][3]
- Serum isopropanol ≥500 mg/dL (83 mmol/L)
- Refractory hypotension despite IV fluids and vasopressors
- Lactic acidosis
- SLED (sustained low-efficiency dialysis) is an alternative if hemodynamically unstable [3]
Critical pearl: Do NOT give fomepizole or ethanol — these block alcohol dehydrogenase and slow isopropanol clearance, worsening toxicity. [1]
17. Disposition
- Admit to ICU: Obtundation/coma, hemodynamic instability, respiratory failure, need for hemodialysis, isopropanol level >150 mg/dL
- Admit to monitored bed: Moderate CNS depression, persistent vomiting, hemodynamic abnormalities responding to fluids
- Observation (6–8 hours): Mild ingestions with improving mental status, stable vitals, tolerating PO
- Discharge criteria: Asymptomatic after observation period, normal vitals, ambulatory, tolerating PO, no suicidal ideation
- Psychiatry consultation: Mandatory for all intentional ingestions before discharge
- Toxicology/Poison Control consultation: Recommended for all significant exposures [7]
- Nephrology consultation: If hemodialysis is being considered [8]
18. Follow Up / Return Precautions
- Follow-up timing: PCP within 48–72 hours; psychiatry follow-up if intentional ingestion
- Return immediately for: Recurrent vomiting, abdominal pain, confusion, dizziness, difficulty breathing, bloody vomit
- Expected recovery: Most patients recover fully within 24–48 hours with supportive care [2]
- Patient counseling:
- Isopropanol is not a safe substitute for ethanol
- Secure household products away from children
- Substance use disorder resources if applicable
- Safety planning if intentional ingestion
References
1. Toxic Alcohols. — Kraut JA, Mullins ME. The New England Journal of Medicine. 2018.
2. Isopropanol Poisoning. — Slaughter RJ, Mason RW, Beasley DM, Vale JA, Schep LJ. Clinical Toxicology. 2014.
3. Sustained Low-Efficiency Dialysis (SLED) Therapy Following Ingestion of Isopropanol in a Pediatric Patient. — Edelen KL, Barton A, Banner W. Clinical Toxicology. 2020.
4. Postmortem Diagnosis of Ketoacidosis: Levels of Beta-Hydroxybutyrate, Acetone and Isopropanol in Different Causes of Death. — Eriksson Hydara Y, Zilg B. Forensic Science International. 2020.
5. Toxic Alcohol Ingestions: Clinical Features, Diagnosis, and Management. — Kraut JA, Kurtz I. Clinical Journal of the American Society of Nephrology : CJASN. 2008.
6. Initial Management of Ingestions of Toxic Substances. — Kulig K. The New England Journal of Medicine. 1992.
7. Acute Medication Poisoning. — Vega IL, Griswold MK, Laskey D. American Family Physician. 2024.
8. Management of Poisonings and Intoxications. — Ghannoum M, Roberts DM. Clinical Journal of the American Society of Nephrology : CJASN. 2023.