Isopropyl alcohol toxicity: Difference between revisions
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== Background == | ==Background== | ||
* | *Main component of rubbing alcohol | ||
*Lethal Dose: 4-8 g/kg or | *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<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 | |||
== Work-Up == | ==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 | |||
{{Sedatve/hypnotic toxicity types}} | |||
==Evaluation== | |||
===Work-Up=== | |||
*Fingerstick glucose | *Fingerstick glucose | ||
*Complete metabolic panel | *Complete metabolic panel | ||
*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 | ||
== | ===Evaluation=== | ||
*Osmolal gap > 10; see [[Osmolal or Osmolar Gap]] | |||
*Osmolal gap > 10 | |||
*Absence of anion gap | *Absence of anion gap | ||
*Absence of metabolic acidosis | *Absence of metabolic acidosis | ||
*Absence of serum beta hydroxybutyrate | *Absence of serum beta hydroxybutyrate | ||
*Presence of serum and urine ketones | *Presence of serum and urine ketones | ||
**Consider other diagnosis if absent | **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}} | |||
== | ==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== | ||
* | *[[Toxic alcohols]] | ||
* | *[[In-Training Exam Review]] | ||
== | ==References== | ||
<references/> | |||
[[Category: | [[Category:Toxicology]] |
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