Isopropyl alcohol toxicity
(Redirected from Isopropanol Toxicity)
Background
- Main component of rubbing alcohol
- Hallmark is osmolar gap, ketosis, that is without acidosis
- Metabolized to acetone, not to an acid
- Takes 30-60 min for acetone to appear in blood; 3 hr to appear in urine
- Lethal Dose: 4-8 g/kg or 250 mL in average adult (calculated using volume of pure isopropyl alcohol)
- Typical store bought rubbing alcohol is 70% isopropyl alcohol by volume, so lethal dose is ~ 350 mL
Pharmacology[1]
- Unlike other toxic alcohols (methanol, ethylene glycol), toxic effects caused by parent agent (IA) rather than metabolite (acetone)
- Metabolized to acetone by alcohol dehydrogenase
- Maximal distribution in ≤ 2 hours
- Lethal dose > 200 mg/dL, although variable literature
Clinical Features
- CNS depression
- Similar to ETOH intoxication, but longer-lasting
- Usually peaks in first hour of ingestion
- GI
- Nausea/vomiting / abdominal pain / hemorrhagic gastritis
- Respiratory depression
- Fruity breath from acetone
- Hypotension, hypothermia from peripheral vasodilation
- Hypoglycemia (in malnourished patients)
Differential Diagnosis
- Starvation ketoacidosis
- Diabetic Ketoacidosis
- Inborn errors of metabolism
- Salicylate Toxicity
- Acetone ingestion
Sedative/hypnotic toxicity
- Absinthe
- Barbiturates
- Benzodiazepines
- Chloral hydrate
- Gamma hydroxybutyrate (GHB)
- Baclofen toxicity
- Opioids
- Toxic alcohols
- Xylazine toxicity
Evaluation
Work-Up
- Fingerstick glucose
- Complete metabolic panel
- Serum ketones
- Serum Osmolality
- Urinalysis
- VBG
- Aspirin/Tylenol levels
- ECG
- Serum isopropyl alcohol level (if available)
- Total CK
Evaluation
- Osmolal gap > 10; see Osmolal or Osmolar Gap
- Absence of anion gap
- Absence of metabolic acidosis
- Absence of serum beta hydroxybutyrate
- Presence of serum and urine ketones
- Consider other diagnosis if absent 2hr after ingestion
- Creatinine may be falsely elevated due to acetone interference with laboratory measurement of Cr
Toxic Alcohols Anion/Osmolar Gaps
Osmolar gap | Metabolic acidosis | Osmolar gap | Anion gap | Ketones | Ca Oxolate stones | Reduced vision | Management |
---|---|---|---|---|---|---|---|
Ethanol | + | + | + (if ketoacidosis) | + | - | Mainly supportive | |
Ethylene glycol | + | + | + | - | + | - | Fomepizole, Thiamine, Pyridoxine, +/- Dialysis |
Methanol | + | + (early on, then disappears) | + | - | - | + | Fomepizole or ethanol, Folinic acid, +/- Dialysis |
Isopropyl alcohol | - | + | - | + | - | + | Mainly supportive |
Propylene gylcol | + | + (initially) | + (converted to lactate) | - | - | - |
Management
- Treatment is supportive.
- No role for fomepizole or ethanol
- Blockade of alcohol dehydrogenase (ADH) will prolong intoxication
- Hemodialysis indications:
- Hypotension
- Comatose
- Consider if IA serum level >200mg/dL
Disposition
- Generally may be discharged once clinically sober.
See Also
References
- ↑ Kraut JF, Kurtz I. Clin J Am Soc Nephrol 2008. PMID: 18045860