Isopropyl alcohol toxicity: Difference between revisions
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==Background== | ==Background== | ||
*Main component of rubbing alcohol | *Main component of rubbing alcohol | ||
*Hallmark is osmolar gap without acidosis | *Hallmark is osmolar gap, ketosis, that is without acidosis | ||
**Metabolized to acetone, not to an acid | **Metabolized to acetone, not to an acid | ||
*Takes 30-60 min for acetone to appear in blood; 3 hr to appear in urine | *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) | *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 | **Typical store bought rubbing alcohol is 70% isopropyl alcohol by volume, so lethal dose is ~ 350 mL | ||
==Pharmacology<ref>Kraut JF, Kurtz I. Clin J Am Soc Nephrol 2008. PMID: 18045860</ref>== | |||
*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== | ==Clinical Features== | ||
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**[[Nausea/vomiting]] / [[abdominal pain]] / hemorrhagic gastritis | **[[Nausea/vomiting]] / [[abdominal pain]] / hemorrhagic gastritis | ||
*Respiratory depression | *Respiratory depression | ||
*[[Hypotension]] | **Fruity breath from acetone | ||
*[[Hypotension]], [[hypothermia]] from peripheral vasodilation | |||
*[[Hypoglycemia]] (in malnourished patients) | *[[Hypoglycemia]] (in malnourished patients) | ||
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{{Sedatve/hypnotic toxicity types}} | {{Sedatve/hypnotic toxicity types}} | ||
== | ==Evaluation== | ||
===Work-Up=== | ===Work-Up=== | ||
*Fingerstick glucose | *Fingerstick glucose | ||
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*Serum ketones | *Serum ketones | ||
*Serum Osmolality | *Serum Osmolality | ||
* | *Urinalysis | ||
*VBG | *VBG | ||
*Aspirin/Tylenol levels | *Aspirin/Tylenol levels | ||
*ECG | *[[ECG]] | ||
*Serum isopropyl alcohol level (if available) | *Serum isopropyl alcohol level (if available) | ||
*Total CK | *Total CK | ||
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*Presence of serum and urine ketones | *Presence of serum and urine ketones | ||
**Consider other diagnosis if absent 2hr after ingestion | **Consider other diagnosis if absent 2hr after ingestion | ||
*Creatinine may be falsely elevated | *Creatinine may be falsely elevated due to acetone interference with laboratory measurement of Cr | ||
{{Toxic Alcohols Anion/Osmolar Gaps}} | {{Toxic Alcohols Anion/Osmolar Gaps}} | ||
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*Treatment is supportive. | *Treatment is supportive. | ||
*No role for fomepizole or ethanol | *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== | ==Disposition== | ||
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==See Also== | ==See Also== | ||
*[[Toxic alcohols]] | *[[Toxic alcohols]] | ||
*[[In-Training Exam Review]] | |||
==References== | ==References== | ||
Latest revision as of 18:52, 20 February 2021
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 | Anion gap | Management | |
|---|---|---|---|
| Ethanol | + | + if ketoacidosis | Mainly supportive |
| Ethylene glycol | + | + | Fomepizole, Thiamine, Pyridoxine, +/- Dialysis |
| Methanol | + | + | Fomepizole or ethanol, Folinic acid, +/- Dialysis |
| Isopropyl alcohol | + | - | Mainly supportive |
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